AIM:To detect the telomerase activity and c-Myc expression in gastric diseases and to examine the relation between these values and Helicobacter pylori(H pylori)as a risk factor for gastric cancer. METHODS:One hundred...AIM:To detect the telomerase activity and c-Myc expression in gastric diseases and to examine the relation between these values and Helicobacter pylori(H pylori)as a risk factor for gastric cancer. METHODS:One hundred and seventy-one gastric samples were studied to detect telomerase activity using a telomerase polymerase chain reaction enzyme linked immunosorbent assay(PCR-ELISA),and c-Myc expression using immunohistochemistry. RESULTS:The telomerase activity and c-Myc expression were higher in cancers(87.69% and 61.54%)than in noncancerous tissues.They were higher in chronic atrophic gastritis with severe intestinal metaplasia(52.38% and 47.62%)than in chronic atrophic gastritis with mild intestinal metaplasia (13.33% and 16.67%).In chronic atrophic gastritis with severe intestinal metaplasia,the telomerase activity and c-Myc expression were higher in cases with Hpylori infection (67.86% and 67.86%)than in those without infection(21.43% and 7.14%).c-Myc expression was higher in gastric cancer with H pylor/infection(77.27%)than in that without infection(28.57%).The telomerase activity and c-Myc expression were coordinately up-regulated in H pylori infected gastric cancer and chronic atrophic gastritis with severe intestinal metaplasia. CONCLUSION:H pylori infection may influence both telomerase activity and c-Myc expression in gastric diseases, especially in chronic atrophic gastritis.展开更多
Human c-myc cDNA was fused with the hormonebinding domain (HBD) cDNA of murine estrogen receptorgene and the chimeric gene was introduced into the CHOcells. The fusion protein, c-MycER, becomes activatedwhen the synth...Human c-myc cDNA was fused with the hormonebinding domain (HBD) cDNA of murine estrogen receptorgene and the chimeric gene was introduced into the CHOcells. The fusion protein, c-MycER, becomes activatedwhen the synthetic steroid, 4-hydroxy-tamoxifen (OHT),binds HBD. Activated c-MycER, likely c-Myc, can inducequiescent CHO cells reentry into S phase and subsequentcell death under serum-free condition. In addition, theexpression of some proposed c-myc target genes such asODC, MrDb, cad, rcc1 and rc1 were found to increase uponOHT induction before S, phase entry and apoptosis, indicating that these target genes are involved in cell cycleregulation and/or apoptosis control. However, the mutantD106-143c-MycER protein does not have above activities.展开更多
This study was designed using c-myc antisense transcripts to evaluate how alteration of c-myc expression in human myeloid leukemic HL-60 cells could influence the myelomonocytic differentiation and induction of apopto...This study was designed using c-myc antisense transcripts to evaluate how alteration of c-myc expression in human myeloid leukemic HL-60 cells could influence the myelomonocytic differentiation and induction of apoptosis. The recombinant plasmid pDACx expressing antisense transcripts to c-myc fragment containing a part of intron 1 and 137 nt exon 2 was constructed. pDACx was transfected into HL-60 cell line by lipofectin reagent.Cytochemical stainings including NBT reduction, peroxidase and α -NAE as well as detection of CD13 and CD33 antigens by flow cytometric analysis indicated occurrence of myelomonocytic differentiation in cells expressing antisense transcripts to c-myc. DNA degradation measured by DNA gel electrophoresis and typical morphological changes observed under electron microscope proved the switchon of apoptosis in terminally differentiating HL-60 cells.展开更多
Coconut(Cocos nucifera L.),a major oil and fruit crop of the Arecaceae family,is extensively cultivated across the Asia—Pacific region.Despite its agricultural importance,genome assembly in coconut remains challengin...Coconut(Cocos nucifera L.),a major oil and fruit crop of the Arecaceae family,is extensively cultivated across the Asia—Pacific region.Despite its agricultural importance,genome assembly in coconut remains challenging due to its large genome size and high proportion of repetitive sequences.Allele-specific expression(ASE)plays a key role in regulating plant development and evolution,yet research on ASE in coconut is limited(Shao et al.,2019;Li et al.,2021;Zhang et al.,2021;Hu et al.,2022).Among phenotypic traits,fruit color is especially important as an indicator of maturity,guiding harvest timing and post-harvest processes(Kapoor et al.,2022).While prior studies have explored various coconut traits such as salt tolerance,fiber content,and plant height(Wang et al.,2021;Yang et al.,2021),investigations into ASE and fruit color remain scarce.展开更多
AIM:To investigate whether abnormal expression of β-catenin in conjunction with overexpression of cyclinD1, c-myc and matrix metalloproteinase-7 (MMP-7) correlated with the carcinogenesis, metastasis and prognosis of...AIM:To investigate whether abnormal expression of β-catenin in conjunction with overexpression of cyclinD1, c-myc and matrix metalloproteinase-7 (MMP-7) correlated with the carcinogenesis, metastasis and prognosis of pancreatic cancer, and to analyze the relationship of β-catenin expression with cyclinDl, c-myc and MMP-7 expression. METHODS: Using immunohistochemistry,we examined the expression of β-catenin, cyclinD1,c-myc and MMP-7 in 47 pancreatic adenocarcinoma tissues, 12 pancreatic intraepithelial neoplasia (PanIN) and 10 normal pancreases, respectively. Proliferation cell nuclear antigen was also tested as the index of proliferative activity of pancreatic cancer cells. RESULTS: In 10 cases of normal pancreatic tissues, epithelial cells showed equally strong membranous expression of β-catenin protein at the cell-cell boundaries, but the expression of cyclinDl, c-myc and MMP-7 was negative. The expression of β-catenin, cyclinD1, c-myc and MMP-7 in PanIN and pancreatic adenocarcinoma tissues had no significant difference [6/12 and 32/47 (68.1%), 6/12 and 35/47 (74.5%), 5/12 and 33/47 (70.2%), 7/12 and 30/47 (63.8%), respectively]. The abnormal expression of β-catenin was significantly correlated to metastasis and one-year survival rate of pancreatic cancer, but had no relation with size, differentiation and cell proliferation. The expression of cyclinD1 was correlated with cell proliferation and extent of differentiation, but not with size, metastasis and one-year survival rate of the pancreatic cancer. The expression of c-myc was not correlated with size, extent of differentiation, metastasis and 1-year survival rate, but closely with cell proliferation of pancreatic cancer. The overexpression of MMP-7 was significantly associated with metastasis and 1-year survival rate of pancreatic cancer,but not with size, extent of differentiation and cell proliferation.There was a highly significant positive association between abnormal expression of β-catenin and overexpression of cyclinD1, c-myc and MMP-7 not only in PanIN (r= 1.000, 0.845, 0.845), but also in pancreatic cancer (r= 0.437, 0.452, 0.435). CONCLUSION: The abnormal expression of β-catenin plays a key role in the carcinogenesis and progression of human pancreatic carcinoma by up-regulating the expression of cyclinDl, c-myc and MMP-7, resulting in the degradation of extracellular matrix and uncontrolled cell proliferation and differentiation,β-catenin abnormal expression and MMP-7 overexpression may be considered as two useful markers for determining metastasis and prognosis of human pancreatic cancer.展开更多
AIM： To investigate the interrelationship of Epstein-Barr virus （EBV） and EBV- encoded proteins with Helicobacter pylori （H pylor/~ infection and the expression of c-met and c-myc oncogene proteins in gastric carc...AIM： To investigate the interrelationship of Epstein-Barr virus （EBV） and EBV- encoded proteins with Helicobacter pylori （H pylor/~ infection and the expression of c-met and c-myc oncogene proteins in gastric carcinoma, and to explore their role in gastric carcinogenesis. METHODS： One hundred and eighty-five gastric carcinoma tissues were detected by polymerase chain reaction （PCR）-Southern blot for EBV genome and in situ hybridization （ISH） for EBV-encoded small RNA 1 （EBER1）. Gastric carcinoma with positive EBER1 signals was confirmed EBV-associated gastric carcinoma （EBVaGC）. The status of Hpylori infection in 185 gastric carcinomas was assessed by rapid urease test and PCR. The samples with positive PCR and urease test were defined as H pylorl infection. The expression of c-met and c-myc oncogene proteins in tissues of EBVaGC and matched EBV-negative gastric carcinoma （EBVnGC） were examined by immunohistochemistry. RT-PCR and Southern hybridization were used to detect the expression of nuclear antigens （EBNAs） 1 and 2, latent membrane protein （LMP） 1, early genes BARF1 and BHRF1 in EBVaGC cases. RESULTS： The positive rate of H pylori and EBV in 185 gastric carcinomas was 59.45% （110/185） and 7.03% （13/185） respectively. No difference was found in sex, age, pathological differentiation, clinical stages and lymph node metastasis between H pylori-positive and H pylori-negative gastric carcinomas. However, the positive rate of H pylori infection in the antrum gastric carcinomas was higher than that of cardia and body gastric carcinomas. In our series, age, pathological differentiation, clinical stages, lymph node metastasis and location of cancer were not different between EBVnGC and EBVaGC, while the positive rate of EBV in male patients was significantly higher than that of female patients. The positivity of Hpylori in EBV-associated and EBV-negative gastric carcinomas was 46.15% （6/13） and 81.40%（104/172） respectively. There was no significant correlation between EBV and H pylori infection. The c-met overexpression was significantly higher in the EBVaGC group than in the EBVnGC group. However, c-met and c-myc expression did not show significant difference between the two groups. Transcripts of EBNA1 were detected in all 13 EBVaGCs, while both EBNA2 and LMP1 mRNA were not detected. Six of the 13 cases exhibited BARF1 transcripts and 2 exhibited BHRF1 transcripts. CONCLUSION： The positivity of H pylori in EBVnGCs is higher than that of EBVaGCs, but no significant correlation is found between EBV infection and H pylori infection. H pylori-positive gastric carcinoma is predominant in antrum location, while EBVaGC has a tendency of predominance in cardia/body location. EBV infection is associated with c-met abnormal expression but not with c-myc protein in EBVaGC. c-met overexpression is not induced by LMP1. BARF1 and BHRF1 may play important roles in the tumorigenesis of EBVaGC through different pathways.展开更多
A human esophageal cancer cell line (EC8712) expressing high-level Myc protein was infected with recombmant retroviral particles (pA-BD9) at a multiplicity of infection (MOI) 1:1. This viral particle contains a neomyc...A human esophageal cancer cell line (EC8712) expressing high-level Myc protein was infected with recombmant retroviral particles (pA-BD9) at a multiplicity of infection (MOI) 1:1. This viral particle contains a neomycin-resistant gene and a 1.53-kb antisense RNA spanning the 2nd exon and its flanking sequences of the human c-myc oncogene. The G418-resistant EC8712 clones showed an 86% inhibition of growth rate and morphological changes characteristic of terminal differentiation and apoptosis. A decrease of about 80% of Myc protein was also observed in these infected cells by ABC-ELISA assay. 12-24 h after the infection of ECS712 cells with pA-BD9 at a high viral particle concentration (MOI = 1:10), the integration of the extrinsic 1.53-kb antisense c-myc fragment into the cancer cell genome was evidenced by the Southern blot analysis. Northern blot analyses showed the expression of this antisense fragment and a decrease of the intrinsic c-myc expression by 74% in comparison with that of the parental EC8712 cells. Heterotransplants of the infected EC8712 cells into the nude mice revealed a substantial decrease in tumorigemcity and morphological changes characteristic of terminal differentiation and apoptosis. Primary monolayer cell cultures of normal epithelia derived from the fetal and adult esophagus mucosa were set as controls. No noticeable increase in c-myc expression was found in these cultures Infection of these cells with the same recombinant viral particles neither affected the growth rate of the cells nor their normal morphology. Our experiments indicate that the drastic decrease of the over-expressed Myc protein in cancer cells may also be an entrance to one of many pathways leading to the terminal differentiation and programmed cell death.展开更多
AIM: To investigate the possible roles of p53 and C-mycgenes in the primary hepatocellular carcinogenesis and therelationship between the liver hyperplastic nodule(LHN) andhepatocellular carcinoma(HCC).METHODS: The ex...AIM: To investigate the possible roles of p53 and C-mycgenes in the primary hepatocellular carcinogenesis and therelationship between the liver hyperplastic nodule(LHN) andhepatocellular carcinoma(HCC).METHODS: The expression of p53 and C-myc genes wasdetected immunohist-ochemically in 73 and 60 cases of HCCand pericarcinomatous tissues, respectively .RESULTS: The positive expression of p53 in HCC wassignificantly higher than that in pericarcinomatous tissues(P＜0.05). In pericarcinomatous tissues, the p53 expressionwas observed only in LHN, but not in liver cirrhosis (LC) andnormal liver tissues. The positive expression rate of C-mycin HCC or LHN was significantly higher than that in LC ornormal liver tissues (P＜0.05 and P＜0.01), however, nosignificant difference was found between HCC and LHN(P＞0.05). The positive expression rate of p53 and C-myc inHCC was correlated with the histological differentiation, thatin the poorly differentiated was significantly higher than thatin well differentiated samples (P＜0.05).CONCLUSION: The overexpression of p53 and C-myc genesmight play a role in the carcinogenesis of HCC; And LHNseems a preneoplastic lesion related to hepatocarcinogenesis;No evidence supports that LC contribute directly to thehepatocarcinogenesis.展开更多
AIM: To investigate chromosome 8 numerical aberra- tions, C-MYC oncogene alterations and its expression in gastric cancer and to correlate these findings with histo- pathological characteristics of gastric tumors. MET...AIM: To investigate chromosome 8 numerical aberra- tions, C-MYC oncogene alterations and its expression in gastric cancer and to correlate these findings with histo- pathological characteristics of gastric tumors. METHODS: Specimens were collected surgically from seven patients with gastric adenocarcinomas. Immu- nostaining for C-MYC and dual-color fluorescence in situ hybridization (FISH) for C-MYC gene and chromosome 8 centromere were performed. RESULTS: All the cases showed chromosome 8 aneu- ploidy and C-MYC amplification, in both the diffuse and intestinal histopathological types of Lauren. No significant difference (P < 0.05) was observed between the level ofchromosome 8 ploidy and the site, stage or histological type of the adenocarcinomas. C-MYC high amplification, like homogeneously stained regions (HSRs) and double minutes (DMs), was observed only in the intestinal-type. Structural rearrangement of C-MYC, like translocation, was observed only in the diffuse type. Regarding C-MYC gene, a significant difference (P < 0.05) was observed between the two histological types. The C-MYC protein was expressed in all the studied cases. In the intestinal- type the C-MYC immunoreactivity was localized only in the nucleus and in the diffuse type in the nucleus and cytoplasm. CONCLUSION: Distinct patterns of alterations between intestinal and diffuse types of gastric tumors support the hypothesis that these types follow different genetic path- ways.展开更多
BACKGROUND: This study was designed to assess theroles of oval cells and c-myc mRNA in the process of hepa-tocarcinogenesis and to clarify the function of carcinogenec-myc in the development of hepatocellular carcinom...BACKGROUND: This study was designed to assess theroles of oval cells and c-myc mRNA in the process of hepa-tocarcinogenesis and to clarify the function of carcinogenec-myc in the development of hepatocellular carcinoma( HCC) and the mechanism of inhibitory function of uscha-ridin on HCC in mouse hepatocarcinogenesis.METHODS: A total of 120 clean SD mice were divided intonormal group, cancer induction group, and interventiongroup. The normal group was fed with standard foragewhile the rest two groups were given p-dimethylaminoazo-benzene (DAB) to induce cancer. Thirteen weeks after in-duction of cancer, the two groups were fed with standardforage and water. Once the pattern was set up, the inter-vention group was given uscharidin injection into the ab-dominal cavity from the first week to the 14th week. Onthe 2nd, 4th, 6th, 8th, 10th, 12th, 14th, 16th, 18th, 20th,22nd, and 24th week, all mice were killed and biopsiedfrom the liver lobe for pathological analysis. At the sametime, the number of tumor nodes was counted and the ex-pression of c-myc mRNA was tested by RT-PCR.RESULTS: Since the 2nd week after cancer induction, pro-liferated oval cells could be seen in the portal area. Initially,the oval cells appeared in the cortical layer of the portalarea, then proliferated gradually and immigrated into theliver parenchyma. In the period of fibrosis after liver proli-feration, proliferated heaps of oval cells were noted in bothportal and peripheral areas. In the period of carcinomatouschange, oval cells could be seen both outside and inside ofcancer nodes, but most of them were distributed outside.The c-myc gene was expressed negatively in the liver tissueof mice. The quantity of the expression began to increaseat the time of infection of the liver and tended to increasewith the degree of hepatic injury. In the period of cancera-tion, the expression level of c-myc mRNA increased gra-dually. The intervention of uscharidin could not inhibit butdelay the increase of the expression of c-myc mRNA.CONCLUSION: Oval cells are closely related to hepatocar-cinoma cells, which play an important role in the occur-rence and development of hepatocarcinogenesis. Uschari-din can inhibit the occurrence of hepatocarcinogenesis orlocal spreading at the early stage of cancer induction byDAB, but it cannot inhibit the expression of c-myc.展开更多
Objective To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes. Methods Sodium selenite at the doses of 5, 10, and 20 μmol/kg was given to rats by i.p. a...Objective To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes. Methods Sodium selenite at the doses of 5, 10, and 20 μmol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was detected by single cell gel electrophoresis （or comet assay）. Hepatocellular apoptosis was determined by TUNEL （TdT-mediated dUTP nick end labelling） and flow cytometry. C-myc, c-fos, and c-jun expression in rat bepatocytes were assayed by Northern dot hybridization. C-myc, c-fos, and c-jun protein were detected by immunohistochemical method. Results At the doses of 5, 10, and 20μmol/kg, DNA damage was induced by sodium selenite in rat hepatocytes and the rates of comet cells were 34.40%, 74.80%, and 91.40% respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the doses of sodium selenite （r=0.9501, P〈0.01）. Sodium selenite at the doses of 5, 10, and 20μmol/kg caused c-myc, c-fos, and c-jun overexpression obviously. The positive brown-yellow signal for proteins of c-myc, c-fos, and c-jun was mainly located in the cytoplasm of bepatocytes with immunohistocbemical method. TUNEL-positive cells were detected in selenium-treated rat livers. Apoptotic rates （%） of selenium-treated liver cells at the doses of 5, 10, and 20 μmol/kg were （3.72±1.76）, （5.82±1.42）, and （11.76±1.87） respectively, being much higher than those in the control. Besides an obvious dose-response relationship between apoptotic rates and the doses of sodium selenite （r=0.9897, P〈0.01）, these results displayed a close relationship between DNA damage rates and apoptotic rates, and the relative coefficient was 0.9021, P〈0.01. Conclusion Selenium at 5-20μmol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.展开更多
Objective： To investigate the expression of Wnt-1, beta-catenin and c-myc in normal ovarian epithelial cell and malignant ovarian epithelial tumor. Methods： Immunohistochemical staining with SP method was conducted ...Objective： To investigate the expression of Wnt-1, beta-catenin and c-myc in normal ovarian epithelial cell and malignant ovarian epithelial tumor. Methods： Immunohistochemical staining with SP method was conducted to identify the expression of Wnt-1, beta-catenin and c-myc in 18 samples of normal epithelial tissue and 34 cases of malignant epithelial tumor of ovary. Results： The expression rate of Wnt-1 and c-myc in malignant epithelial tumors was higher than those in normal epithelial cell （P〈0.05）. The abnormal expression rate of beta-catenin in malignant ovarian epithelial tumors was higher than that in normal epithelial cell （P〈0.05）. A significant positive correlation was found between Wnt-1, beta-catenin and c-myc in malignant ovarian epithelial tumor （P〈0.05）. A significant difference of expressions of Beta-catenin and C-myc was found between serous and mucinous tumors （P〈0.05）. Conclusion： The abnormal expression of Wnt-1, beta-catenin and c-myc might indicate the malignant transformation in ovarian epithelial tumors.展开更多
AIM:To rapidly detect molecular alterations in different malignancies and investigate the possible role of Tp53,C-myc,and CCND1 genes in development of tumors in human organs and their adjacent normal tissues,as well ...AIM:To rapidly detect molecular alterations in different malignancies and investigate the possible role of Tp53,C-myc,and CCND1 genes in development of tumors in human organs and their adjacent normal tissues,as well as the possible relation between well-and poorly-differentiated tumors.METHODS:A tissue array consisting of seven different tumors was generated.The tissue array included 120 points of esophagus,120 points of stomach,80 points of rectum,60 points of thyroid gland,100 points of mammary gland,80 points of liver,and 80 points of colon.Expressions of Tp53,C-myc,and CCND1 were determined by RNA in situ hybridization.3' terminal digoxin-labeled anti-sense single stranded oligonucleotide and locked nucleic acid modifying probe were used.RESULTS:The expression level of Tp53 gene was higher in six different carcinoma tissue samples than in paracancerous tissue samples with the exception in colon carcinoma tissue samples(P < 0.05).The expression level of CCND1 gene was significantly different in different carcinoma tissue samples with the exception in esophagus and colon carcinoma tissue samples.The expression level of C-myc gene was different in esophagus carcinoma tissue samples(c2 = 18.495,P = 0.000),stomach carcinoma tissue samples(c2 = 23.750,P = 0.000),and thyroid gland tissue samples(c2 = 10.999,P = 0.004).The intensity of signals was also different in different carcinoma tissue samples and paracancerous tissue samples.CONCLUSION:Over-expression of the Tp53,CCND1,and C-myc genes appears to play a role in development of human cancer by regulating the expression of mRNA.Tp53,CCND1 and C-myc genes are significantly correlated with the development of different carcinomas.展开更多
Artificial intelligence,such as deep learning technology,has advanced the study of facial expression recognition since facial expression carries rich emotional information and is significant for many naturalistic situ...Artificial intelligence,such as deep learning technology,has advanced the study of facial expression recognition since facial expression carries rich emotional information and is significant for many naturalistic situations.To pursue a high facial expression recognition accuracy,the network model of deep learning is generally designed to be very deep while the model’s real-time performance is typically constrained and limited.With MobileNetV3,a lightweight model with a good accuracy,a further study is conducted by adding a basic ResNet module to each of its existing modules and an SSH(Single Stage Headless Face Detector)context module to expand the model’s perceptual field.In this article,the enhanced model named Res-MobileNetV3,could alleviate the subpar of real-time performance and compress the size of large network models,which can process information at a rate of up to 33 frames per second.Although the improved model has been verified to be slightly inferior to the current state-of-the-art method in aspect of accuracy rate on the publically available face expression datasets,it can bring a good balance on accuracy,real-time performance,model size and model complexity in practical applications.展开更多
Objective:To explore the expressions of c-fos and c-myc in skin lesion of cutaneous squamous cell carcinoma(CSCC).Methods:Using retrospective analysis.73 cases of CSCC were selected from Department of Dermatology,the ...Objective:To explore the expressions of c-fos and c-myc in skin lesion of cutaneous squamous cell carcinoma(CSCC).Methods:Using retrospective analysis.73 cases of CSCC were selected from Department of Dermatology,the Second Affiliated Hospital of Xi'an Jiaotong University.which were removed between January 2000 and January 2012.It was considered as experimental group.Meanwhile.11 cases of normal skin specimens of non tumor patients were selected as control group.The expression level of c-fos and c-myc was compared in the two groups.Results:The expressions of c-fos[72.60%(53/73)]and c-myc[83.56%(61/73)]in experimental group were statistically significant(P≤0.05)compared with control group(0%).Expression of c-myc protein was negatively related to differentiation of CSCC.The difference was statistically significant(X^2=7.26.P=0.001<0.05).While expression of c-fos protein was positively related to differentiation of CSCC.which was statistically significant(X^2=7.47,P=0.0012<0.025).Conclusions:The expression level of c-fos and c-myc can be used as an importan indicator of CSCC differentiation,and it has closely connection with the differentiated degree,which can guide clinical prognosis.展开更多
This study investigated the effect of cadmium on the telomerase activity,the expression of TERT,c-myc and p53 and the apoptosis of rat hepatocytes.The rats were administrated 5,10 and 20 μmol/kg cadmium chloride intr...This study investigated the effect of cadmium on the telomerase activity,the expression of TERT,c-myc and p53 and the apoptosis of rat hepatocytes.The rats were administrated 5,10 and 20 μmol/kg cadmium chloride intraperitoneally and sacrificed 48 h after the initial treatment.The telomerase activity of the rat hepatocytes was measured by the telomeric repeat amplification protocol (TRAP),and apoptosis was detected by flow cytometry.The mRNA expressions of TERT,c-myc and p53 were measured by reverse transcription-polymerase chain reaction (RT-PCR).C-myc and P53 proteins were determined by immunochemistry.The results showed that cadmium chloride increased the hepatocellular telomerase activity in a dose-dependant manner and induced the apoptosis of hepatocytes significantly.The value of relative coefficient between the telomerase activity and the apoptosis rate was 0.9398.RT-PCR revealed that specific bands corresponding to the TERT mRNA,c-myc mRNA,and p53 mRNA were displayed at 185,342 and 538 bp respectively.Cadmium chloride could substantially increase the mRNA expressions of TERT,c-myc and p53 in rat hepatocytes,as compared with control.Moreover,cadmium chloride at the doses of 5,10 and 20 μmol/kg could increase the content of P53 protein in rat hepatocytes obviously,but only that at the doses of 10 and 20 μmol/kg substantially promoted the c-myc protein level in rat hepatocytes.Our study herein suggested that cadmium may contribute to the carcinogenesis by activating telomerase,and overexpressing the mRNAs of TERT,c-myc and p53,and causing apoptosis of normal cells.展开更多
The role of growth factors and proto-oncogene in pulmonary vascular structural remodelling is not well known.The present study examined gene expression of platelet-derived growth factor(PDGF)-A and -B chain and proto-...The role of growth factors and proto-oncogene in pulmonary vascular structural remodelling is not well known.The present study examined gene expression of platelet-derived growth factor(PDGF)-A and -B chain and proto-oncogene,c-myc,in lung tissue and pulmonary artery of rats exposed to hypoxia and compared to those levels of gene expression in normal rats.Normal lungs and pulmonary artery expressed PDGF-A chain transcript of 1.7 kb and PDGF-B chain transcript of 3.5 Kb.The c-myc transcript of 2.2 kb was expressed as well. After hypoxic exposure for 7 and 14 days mRNA levels of PDGF-B chain and cmyc were elevated significantly compared with those of control rats.PDGF-A chain mRNA increased after hypoxia for 7 days,and then declined.These results suggest that activation of autocrine and/or paracrine is important in proliferation mechanism of pulmonary artery smooth muscle cells in hypoxic pulmonary hypertensive rats.展开更多
AIM： To evaluate the effect of hydroxyapatite nano- particles （Nano HAP） by intravenous injection on the inhibition of implanted hepatic VX2 tumor growth in rabbits and cell p53/c-Myc protein expression. METHODS： ...AIM： To evaluate the effect of hydroxyapatite nano- particles （Nano HAP） by intravenous injection on the inhibition of implanted hepatic VX2 tumor growth in rabbits and cell p53/c-Myc protein expression. METHODS： 60 hepatic VX2 tumor-bearing rabbits was randomly divided into five groups. Nano HAP collosol 20 mglkg, 40 mg/kg, 5-FU solutions 20 mg/mL, mixed liquor of 5-FU solution 20 mg/mL and Nano HAP collosol 20 mg/kg were infused by vein, normal saline conducted as the control. The general state, weight, liver function and gross tumor volume were detected dynamically. The expression of p53 and c-Myc gene protein in tumor tissue was detected by immunohistochemistry methods. RESULTS： The growth of implanted hepatic VX2 tumors was significantly inhibited in all therapy groups, 3 wk after the injection, the tumor control rates in Nano HAP collosol groups were 25.5% and 32.5% respectively, and the gross tumor volumes were obviously less than that of control group. （24.81 ± 5.17 and 22.73 ± 4.23 vs 33.32 ± 5.26, P 〈 0.05）. The tumor control rate of 5-FU group was 43.7% （18.74 4± 4.40 vs 33.32 ± 5.26, P 〈 0.05）, but the general state of the animals after injection aggravated; and the adverse reaction in the drug combination group obviously decreased. Due to the effect of Nano HAP, the positive expression of tumor associated the mutated p53 and c-Myc in tumor tissue was decreased obviously compared with the control group. CONCLUSION： Nano HAP has evident inhibitory action on rabbit implanted hepatic VX2 tumor in vivo, which may be the result of decreasing the expression of the mutated p53 and c-myc, and drug combination can obviously decrease the adverse reaction of 5-FU.展开更多
AIM: To investigate the interrelationship between H pylori and Epstein-Barr virus (EBV) infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc, Bcl-2 and Bax expression. METHODS: sevent...AIM: To investigate the interrelationship between H pylori and Epstein-Barr virus (EBV) infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc, Bcl-2 and Bax expression. METHODS: seventy-one gastric carcinoma tissues were assessed by polymerase chain reaction (PCR) for H pylori and in situ hybridization for EBV. c-Myc, Bcl-2 and Bax expression were detected by immunohistochemistry and single-stranded conformational polymorphism (SSCP) for p53 mutation. RESULTS: The positivity rates for H pylori and EBV were 94.4% and 8.45%, respectively. The majority of the cases displayed only the H pylori presence. All EBV positive cases were also H pylori positive. None infectious agent was observed in 5.55% of the cases. The intestinal type tumor was more frequent in the co-infected and non-infected groups. The female predominated in the non-infected group showing statistical significance (70.4% vs 29.6%, P=0.039). The Bcl-2 was only detected in the group exclusively infected by H pylori. However, c-Myc and Bax were detected in the three groups but with a low frequency in the co-infected group. Mutation of p53 was present in all groups, with the highest frequencies in the H pylori positive groups. CONCLUSION: The frequency of H pylori infection in gastric carcinomas was high. The presented data indicated that gastric carcinogenesis has different pathways depending of the presence of the two investigated infectious agents, suggesting a possible involvement of H pylori with apoptotic process. The low expression of c-Myc and Bax in the EBV-positive groups suggests that EBV may inhibit the expression of these proteins. Nevertheless, p53 mutation shows to be a relevant alteration, independent of both infectious agents.展开更多
文摘AIM:To detect the telomerase activity and c-Myc expression in gastric diseases and to examine the relation between these values and Helicobacter pylori(H pylori)as a risk factor for gastric cancer. METHODS:One hundred and seventy-one gastric samples were studied to detect telomerase activity using a telomerase polymerase chain reaction enzyme linked immunosorbent assay(PCR-ELISA),and c-Myc expression using immunohistochemistry. RESULTS:The telomerase activity and c-Myc expression were higher in cancers(87.69% and 61.54%)than in noncancerous tissues.They were higher in chronic atrophic gastritis with severe intestinal metaplasia(52.38% and 47.62%)than in chronic atrophic gastritis with mild intestinal metaplasia (13.33% and 16.67%).In chronic atrophic gastritis with severe intestinal metaplasia,the telomerase activity and c-Myc expression were higher in cases with Hpylori infection (67.86% and 67.86%)than in those without infection(21.43% and 7.14%).c-Myc expression was higher in gastric cancer with H pylor/infection(77.27%)than in that without infection(28.57%).The telomerase activity and c-Myc expression were coordinately up-regulated in H pylori infected gastric cancer and chronic atrophic gastritis with severe intestinal metaplasia. CONCLUSION:H pylori infection may influence both telomerase activity and c-Myc expression in gastric diseases, especially in chronic atrophic gastritis.
文摘Human c-myc cDNA was fused with the hormonebinding domain (HBD) cDNA of murine estrogen receptorgene and the chimeric gene was introduced into the CHOcells. The fusion protein, c-MycER, becomes activatedwhen the synthetic steroid, 4-hydroxy-tamoxifen (OHT),binds HBD. Activated c-MycER, likely c-Myc, can inducequiescent CHO cells reentry into S phase and subsequentcell death under serum-free condition. In addition, theexpression of some proposed c-myc target genes such asODC, MrDb, cad, rcc1 and rc1 were found to increase uponOHT induction before S, phase entry and apoptosis, indicating that these target genes are involved in cell cycleregulation and/or apoptosis control. However, the mutantD106-143c-MycER protein does not have above activities.
文摘This study was designed using c-myc antisense transcripts to evaluate how alteration of c-myc expression in human myeloid leukemic HL-60 cells could influence the myelomonocytic differentiation and induction of apoptosis. The recombinant plasmid pDACx expressing antisense transcripts to c-myc fragment containing a part of intron 1 and 137 nt exon 2 was constructed. pDACx was transfected into HL-60 cell line by lipofectin reagent.Cytochemical stainings including NBT reduction, peroxidase and α -NAE as well as detection of CD13 and CD33 antigens by flow cytometric analysis indicated occurrence of myelomonocytic differentiation in cells expressing antisense transcripts to c-myc. DNA degradation measured by DNA gel electrophoresis and typical morphological changes observed under electron microscope proved the switchon of apoptosis in terminally differentiating HL-60 cells.
基金supported by Central Public-interest Scientific Institution Basal Research Fund(CATAS-Nos.1630152023007,1630152023011,1630152023012,1630152023013)the National Natural Science Foundation of China(Grant No.32071805).
文摘Coconut(Cocos nucifera L.),a major oil and fruit crop of the Arecaceae family,is extensively cultivated across the Asia—Pacific region.Despite its agricultural importance,genome assembly in coconut remains challenging due to its large genome size and high proportion of repetitive sequences.Allele-specific expression(ASE)plays a key role in regulating plant development and evolution,yet research on ASE in coconut is limited(Shao et al.,2019;Li et al.,2021;Zhang et al.,2021;Hu et al.,2022).Among phenotypic traits,fruit color is especially important as an indicator of maturity,guiding harvest timing and post-harvest processes(Kapoor et al.,2022).While prior studies have explored various coconut traits such as salt tolerance,fiber content,and plant height(Wang et al.,2021;Yang et al.,2021),investigations into ASE and fruit color remain scarce.
基金Supported by the Foundation of Shandong Education Committee,No. 03K02
文摘AIM:To investigate whether abnormal expression of β-catenin in conjunction with overexpression of cyclinD1, c-myc and matrix metalloproteinase-7 (MMP-7) correlated with the carcinogenesis, metastasis and prognosis of pancreatic cancer, and to analyze the relationship of β-catenin expression with cyclinDl, c-myc and MMP-7 expression. METHODS: Using immunohistochemistry,we examined the expression of β-catenin, cyclinD1,c-myc and MMP-7 in 47 pancreatic adenocarcinoma tissues, 12 pancreatic intraepithelial neoplasia (PanIN) and 10 normal pancreases, respectively. Proliferation cell nuclear antigen was also tested as the index of proliferative activity of pancreatic cancer cells. RESULTS: In 10 cases of normal pancreatic tissues, epithelial cells showed equally strong membranous expression of β-catenin protein at the cell-cell boundaries, but the expression of cyclinDl, c-myc and MMP-7 was negative. The expression of β-catenin, cyclinD1, c-myc and MMP-7 in PanIN and pancreatic adenocarcinoma tissues had no significant difference [6/12 and 32/47 (68.1%), 6/12 and 35/47 (74.5%), 5/12 and 33/47 (70.2%), 7/12 and 30/47 (63.8%), respectively]. The abnormal expression of β-catenin was significantly correlated to metastasis and one-year survival rate of pancreatic cancer, but had no relation with size, differentiation and cell proliferation. The expression of cyclinD1 was correlated with cell proliferation and extent of differentiation, but not with size, metastasis and one-year survival rate of the pancreatic cancer. The expression of c-myc was not correlated with size, extent of differentiation, metastasis and 1-year survival rate, but closely with cell proliferation of pancreatic cancer. The overexpression of MMP-7 was significantly associated with metastasis and 1-year survival rate of pancreatic cancer,but not with size, extent of differentiation and cell proliferation.There was a highly significant positive association between abnormal expression of β-catenin and overexpression of cyclinD1, c-myc and MMP-7 not only in PanIN (r= 1.000, 0.845, 0.845), but also in pancreatic cancer (r= 0.437, 0.452, 0.435). CONCLUSION: The abnormal expression of β-catenin plays a key role in the carcinogenesis and progression of human pancreatic carcinoma by up-regulating the expression of cyclinDl, c-myc and MMP-7, resulting in the degradation of extracellular matrix and uncontrolled cell proliferation and differentiation,β-catenin abnormal expression and MMP-7 overexpression may be considered as two useful markers for determining metastasis and prognosis of human pancreatic cancer.
文摘AIM： To investigate the interrelationship of Epstein-Barr virus （EBV） and EBV- encoded proteins with Helicobacter pylori （H pylor/~ infection and the expression of c-met and c-myc oncogene proteins in gastric carcinoma, and to explore their role in gastric carcinogenesis. METHODS： One hundred and eighty-five gastric carcinoma tissues were detected by polymerase chain reaction （PCR）-Southern blot for EBV genome and in situ hybridization （ISH） for EBV-encoded small RNA 1 （EBER1）. Gastric carcinoma with positive EBER1 signals was confirmed EBV-associated gastric carcinoma （EBVaGC）. The status of Hpylori infection in 185 gastric carcinomas was assessed by rapid urease test and PCR. The samples with positive PCR and urease test were defined as H pylorl infection. The expression of c-met and c-myc oncogene proteins in tissues of EBVaGC and matched EBV-negative gastric carcinoma （EBVnGC） were examined by immunohistochemistry. RT-PCR and Southern hybridization were used to detect the expression of nuclear antigens （EBNAs） 1 and 2, latent membrane protein （LMP） 1, early genes BARF1 and BHRF1 in EBVaGC cases. RESULTS： The positive rate of H pylori and EBV in 185 gastric carcinomas was 59.45% （110/185） and 7.03% （13/185） respectively. No difference was found in sex, age, pathological differentiation, clinical stages and lymph node metastasis between H pylori-positive and H pylori-negative gastric carcinomas. However, the positive rate of H pylori infection in the antrum gastric carcinomas was higher than that of cardia and body gastric carcinomas. In our series, age, pathological differentiation, clinical stages, lymph node metastasis and location of cancer were not different between EBVnGC and EBVaGC, while the positive rate of EBV in male patients was significantly higher than that of female patients. The positivity of Hpylori in EBV-associated and EBV-negative gastric carcinomas was 46.15% （6/13） and 81.40%（104/172） respectively. There was no significant correlation between EBV and H pylori infection. The c-met overexpression was significantly higher in the EBVaGC group than in the EBVnGC group. However, c-met and c-myc expression did not show significant difference between the two groups. Transcripts of EBNA1 were detected in all 13 EBVaGCs, while both EBNA2 and LMP1 mRNA were not detected. Six of the 13 cases exhibited BARF1 transcripts and 2 exhibited BHRF1 transcripts. CONCLUSION： The positivity of H pylori in EBVnGCs is higher than that of EBVaGCs, but no significant correlation is found between EBV infection and H pylori infection. H pylori-positive gastric carcinoma is predominant in antrum location, while EBVaGC has a tendency of predominance in cardia/body location. EBV infection is associated with c-met abnormal expression but not with c-myc protein in EBVaGC. c-met overexpression is not induced by LMP1. BARF1 and BHRF1 may play important roles in the tumorigenesis of EBVaGC through different pathways.
文摘A human esophageal cancer cell line (EC8712) expressing high-level Myc protein was infected with recombmant retroviral particles (pA-BD9) at a multiplicity of infection (MOI) 1:1. This viral particle contains a neomycin-resistant gene and a 1.53-kb antisense RNA spanning the 2nd exon and its flanking sequences of the human c-myc oncogene. The G418-resistant EC8712 clones showed an 86% inhibition of growth rate and morphological changes characteristic of terminal differentiation and apoptosis. A decrease of about 80% of Myc protein was also observed in these infected cells by ABC-ELISA assay. 12-24 h after the infection of ECS712 cells with pA-BD9 at a high viral particle concentration (MOI = 1:10), the integration of the extrinsic 1.53-kb antisense c-myc fragment into the cancer cell genome was evidenced by the Southern blot analysis. Northern blot analyses showed the expression of this antisense fragment and a decrease of the intrinsic c-myc expression by 74% in comparison with that of the parental EC8712 cells. Heterotransplants of the infected EC8712 cells into the nude mice revealed a substantial decrease in tumorigemcity and morphological changes characteristic of terminal differentiation and apoptosis. Primary monolayer cell cultures of normal epithelia derived from the fetal and adult esophagus mucosa were set as controls. No noticeable increase in c-myc expression was found in these cultures Infection of these cells with the same recombinant viral particles neither affected the growth rate of the cells nor their normal morphology. Our experiments indicate that the drastic decrease of the over-expressed Myc protein in cancer cells may also be an entrance to one of many pathways leading to the terminal differentiation and programmed cell death.
基金the scientific research fundation of Shandong Provincial Education Committee(J94,K26)
文摘AIM: To investigate the possible roles of p53 and C-mycgenes in the primary hepatocellular carcinogenesis and therelationship between the liver hyperplastic nodule(LHN) andhepatocellular carcinoma(HCC).METHODS: The expression of p53 and C-myc genes wasdetected immunohist-ochemically in 73 and 60 cases of HCCand pericarcinomatous tissues, respectively .RESULTS: The positive expression of p53 in HCC wassignificantly higher than that in pericarcinomatous tissues(P＜0.05). In pericarcinomatous tissues, the p53 expressionwas observed only in LHN, but not in liver cirrhosis (LC) andnormal liver tissues. The positive expression rate of C-mycin HCC or LHN was significantly higher than that in LC ornormal liver tissues (P＜0.05 and P＜0.01), however, nosignificant difference was found between HCC and LHN(P＞0.05). The positive expression rate of p53 and C-myc inHCC was correlated with the histological differentiation, thatin the poorly differentiated was significantly higher than thatin well differentiated samples (P＜0.05).CONCLUSION: The overexpression of p53 and C-myc genesmight play a role in the carcinogenesis of HCC; And LHNseems a preneoplastic lesion related to hepatocarcinogenesis;No evidence supports that LC contribute directly to thehepatocarcinogenesis.
基金Supported by Financiadora de Estudos e Projetos(FINEP CT-INFRA/FADESP),No.0927-03Fundacao de Amparo a Pesquisa do Estado de Sao Paulo(FAPESP)No.2003/06540-5+1 种基金DQC had a master fellowship,No.151127/2002-6granted by Coordenacao de Aperfeicoamento de Pessoal de Nível Superior
文摘AIM: To investigate chromosome 8 numerical aberra- tions, C-MYC oncogene alterations and its expression in gastric cancer and to correlate these findings with histo- pathological characteristics of gastric tumors. METHODS: Specimens were collected surgically from seven patients with gastric adenocarcinomas. Immu- nostaining for C-MYC and dual-color fluorescence in situ hybridization (FISH) for C-MYC gene and chromosome 8 centromere were performed. RESULTS: All the cases showed chromosome 8 aneu- ploidy and C-MYC amplification, in both the diffuse and intestinal histopathological types of Lauren. No significant difference (P < 0.05) was observed between the level ofchromosome 8 ploidy and the site, stage or histological type of the adenocarcinomas. C-MYC high amplification, like homogeneously stained regions (HSRs) and double minutes (DMs), was observed only in the intestinal-type. Structural rearrangement of C-MYC, like translocation, was observed only in the diffuse type. Regarding C-MYC gene, a significant difference (P < 0.05) was observed between the two histological types. The C-MYC protein was expressed in all the studied cases. In the intestinal- type the C-MYC immunoreactivity was localized only in the nucleus and in the diffuse type in the nucleus and cytoplasm. CONCLUSION: Distinct patterns of alterations between intestinal and diffuse types of gastric tumors support the hypothesis that these types follow different genetic path- ways.
基金This work was supported by two grants from the Science Fundation ofGuangdong Province, China (No. 010593 No. 020097).
文摘BACKGROUND: This study was designed to assess theroles of oval cells and c-myc mRNA in the process of hepa-tocarcinogenesis and to clarify the function of carcinogenec-myc in the development of hepatocellular carcinoma( HCC) and the mechanism of inhibitory function of uscha-ridin on HCC in mouse hepatocarcinogenesis.METHODS: A total of 120 clean SD mice were divided intonormal group, cancer induction group, and interventiongroup. The normal group was fed with standard foragewhile the rest two groups were given p-dimethylaminoazo-benzene (DAB) to induce cancer. Thirteen weeks after in-duction of cancer, the two groups were fed with standardforage and water. Once the pattern was set up, the inter-vention group was given uscharidin injection into the ab-dominal cavity from the first week to the 14th week. Onthe 2nd, 4th, 6th, 8th, 10th, 12th, 14th, 16th, 18th, 20th,22nd, and 24th week, all mice were killed and biopsiedfrom the liver lobe for pathological analysis. At the sametime, the number of tumor nodes was counted and the ex-pression of c-myc mRNA was tested by RT-PCR.RESULTS: Since the 2nd week after cancer induction, pro-liferated oval cells could be seen in the portal area. Initially,the oval cells appeared in the cortical layer of the portalarea, then proliferated gradually and immigrated into theliver parenchyma. In the period of fibrosis after liver proli-feration, proliferated heaps of oval cells were noted in bothportal and peripheral areas. In the period of carcinomatouschange, oval cells could be seen both outside and inside ofcancer nodes, but most of them were distributed outside.The c-myc gene was expressed negatively in the liver tissueof mice. The quantity of the expression began to increaseat the time of infection of the liver and tended to increasewith the degree of hepatic injury. In the period of cancera-tion, the expression level of c-myc mRNA increased gra-dually. The intervention of uscharidin could not inhibit butdelay the increase of the expression of c-myc mRNA.CONCLUSION: Oval cells are closely related to hepatocar-cinoma cells, which play an important role in the occur-rence and development of hepatocarcinogenesis. Uschari-din can inhibit the occurrence of hepatocarcinogenesis orlocal spreading at the early stage of cancer induction byDAB, but it cannot inhibit the expression of c-myc.
基金This work was supported by National Natural Science Foundation of China (No. 30271110, 30471500).
文摘Objective To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes. Methods Sodium selenite at the doses of 5, 10, and 20 μmol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was detected by single cell gel electrophoresis （or comet assay）. Hepatocellular apoptosis was determined by TUNEL （TdT-mediated dUTP nick end labelling） and flow cytometry. C-myc, c-fos, and c-jun expression in rat bepatocytes were assayed by Northern dot hybridization. C-myc, c-fos, and c-jun protein were detected by immunohistochemical method. Results At the doses of 5, 10, and 20μmol/kg, DNA damage was induced by sodium selenite in rat hepatocytes and the rates of comet cells were 34.40%, 74.80%, and 91.40% respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the doses of sodium selenite （r=0.9501, P〈0.01）. Sodium selenite at the doses of 5, 10, and 20μmol/kg caused c-myc, c-fos, and c-jun overexpression obviously. The positive brown-yellow signal for proteins of c-myc, c-fos, and c-jun was mainly located in the cytoplasm of bepatocytes with immunohistocbemical method. TUNEL-positive cells were detected in selenium-treated rat livers. Apoptotic rates （%） of selenium-treated liver cells at the doses of 5, 10, and 20 μmol/kg were （3.72±1.76）, （5.82±1.42）, and （11.76±1.87） respectively, being much higher than those in the control. Besides an obvious dose-response relationship between apoptotic rates and the doses of sodium selenite （r=0.9897, P〈0.01）, these results displayed a close relationship between DNA damage rates and apoptotic rates, and the relative coefficient was 0.9021, P〈0.01. Conclusion Selenium at 5-20μmol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.
基金a grant from the Science Foundation of Chongqing Medical University(No.XB0508)
文摘Objective： To investigate the expression of Wnt-1, beta-catenin and c-myc in normal ovarian epithelial cell and malignant ovarian epithelial tumor. Methods： Immunohistochemical staining with SP method was conducted to identify the expression of Wnt-1, beta-catenin and c-myc in 18 samples of normal epithelial tissue and 34 cases of malignant epithelial tumor of ovary. Results： The expression rate of Wnt-1 and c-myc in malignant epithelial tumors was higher than those in normal epithelial cell （P〈0.05）. The abnormal expression rate of beta-catenin in malignant ovarian epithelial tumors was higher than that in normal epithelial cell （P〈0.05）. A significant positive correlation was found between Wnt-1, beta-catenin and c-myc in malignant ovarian epithelial tumor （P〈0.05）. A significant difference of expressions of Beta-catenin and C-myc was found between serous and mucinous tumors （P〈0.05）. Conclusion： The abnormal expression of Wnt-1, beta-catenin and c-myc might indicate the malignant transformation in ovarian epithelial tumors.
基金Supported by Foundation of Xiamen Science and Technology Bureau,Fujian Province,China,No.3502Z20074023
文摘AIM:To rapidly detect molecular alterations in different malignancies and investigate the possible role of Tp53,C-myc,and CCND1 genes in development of tumors in human organs and their adjacent normal tissues,as well as the possible relation between well-and poorly-differentiated tumors.METHODS:A tissue array consisting of seven different tumors was generated.The tissue array included 120 points of esophagus,120 points of stomach,80 points of rectum,60 points of thyroid gland,100 points of mammary gland,80 points of liver,and 80 points of colon.Expressions of Tp53,C-myc,and CCND1 were determined by RNA in situ hybridization.3' terminal digoxin-labeled anti-sense single stranded oligonucleotide and locked nucleic acid modifying probe were used.RESULTS:The expression level of Tp53 gene was higher in six different carcinoma tissue samples than in paracancerous tissue samples with the exception in colon carcinoma tissue samples(P < 0.05).The expression level of CCND1 gene was significantly different in different carcinoma tissue samples with the exception in esophagus and colon carcinoma tissue samples.The expression level of C-myc gene was different in esophagus carcinoma tissue samples(c2 = 18.495,P = 0.000),stomach carcinoma tissue samples(c2 = 23.750,P = 0.000),and thyroid gland tissue samples(c2 = 10.999,P = 0.004).The intensity of signals was also different in different carcinoma tissue samples and paracancerous tissue samples.CONCLUSION:Over-expression of the Tp53,CCND1,and C-myc genes appears to play a role in development of human cancer by regulating the expression of mRNA.Tp53,CCND1 and C-myc genes are significantly correlated with the development of different carcinomas.
基金supported by China Academy of Railway Sciences Corporation Limited(No.2021YJ127).
文摘Artificial intelligence,such as deep learning technology,has advanced the study of facial expression recognition since facial expression carries rich emotional information and is significant for many naturalistic situations.To pursue a high facial expression recognition accuracy,the network model of deep learning is generally designed to be very deep while the model’s real-time performance is typically constrained and limited.With MobileNetV3,a lightweight model with a good accuracy,a further study is conducted by adding a basic ResNet module to each of its existing modules and an SSH(Single Stage Headless Face Detector)context module to expand the model’s perceptual field.In this article,the enhanced model named Res-MobileNetV3,could alleviate the subpar of real-time performance and compress the size of large network models,which can process information at a rate of up to 33 frames per second.Although the improved model has been verified to be slightly inferior to the current state-of-the-art method in aspect of accuracy rate on the publically available face expression datasets,it can bring a good balance on accuracy,real-time performance,model size and model complexity in practical applications.
基金Supported by Natural Science Foundation of Shaanxi Province(Grant No.2018722)
文摘Objective:To explore the expressions of c-fos and c-myc in skin lesion of cutaneous squamous cell carcinoma(CSCC).Methods:Using retrospective analysis.73 cases of CSCC were selected from Department of Dermatology,the Second Affiliated Hospital of Xi'an Jiaotong University.which were removed between January 2000 and January 2012.It was considered as experimental group.Meanwhile.11 cases of normal skin specimens of non tumor patients were selected as control group.The expression level of c-fos and c-myc was compared in the two groups.Results:The expressions of c-fos[72.60%(53/73)]and c-myc[83.56%(61/73)]in experimental group were statistically significant(P≤0.05)compared with control group(0%).Expression of c-myc protein was negatively related to differentiation of CSCC.The difference was statistically significant(X^2=7.26.P=0.001<0.05).While expression of c-fos protein was positively related to differentiation of CSCC.which was statistically significant(X^2=7.47,P=0.0012<0.025).Conclusions:The expression level of c-fos and c-myc can be used as an importan indicator of CSCC differentiation,and it has closely connection with the differentiated degree,which can guide clinical prognosis.
基金supported by the National Natural Sciences Foundation of China(No.30271110)Scientific Foundation(No.2006GGW01)Teacher's Foundation of Guangdong Pharmaceutical University,China
文摘This study investigated the effect of cadmium on the telomerase activity,the expression of TERT,c-myc and p53 and the apoptosis of rat hepatocytes.The rats were administrated 5,10 and 20 μmol/kg cadmium chloride intraperitoneally and sacrificed 48 h after the initial treatment.The telomerase activity of the rat hepatocytes was measured by the telomeric repeat amplification protocol (TRAP),and apoptosis was detected by flow cytometry.The mRNA expressions of TERT,c-myc and p53 were measured by reverse transcription-polymerase chain reaction (RT-PCR).C-myc and P53 proteins were determined by immunochemistry.The results showed that cadmium chloride increased the hepatocellular telomerase activity in a dose-dependant manner and induced the apoptosis of hepatocytes significantly.The value of relative coefficient between the telomerase activity and the apoptosis rate was 0.9398.RT-PCR revealed that specific bands corresponding to the TERT mRNA,c-myc mRNA,and p53 mRNA were displayed at 185,342 and 538 bp respectively.Cadmium chloride could substantially increase the mRNA expressions of TERT,c-myc and p53 in rat hepatocytes,as compared with control.Moreover,cadmium chloride at the doses of 5,10 and 20 μmol/kg could increase the content of P53 protein in rat hepatocytes obviously,but only that at the doses of 10 and 20 μmol/kg substantially promoted the c-myc protein level in rat hepatocytes.Our study herein suggested that cadmium may contribute to the carcinogenesis by activating telomerase,and overexpressing the mRNAs of TERT,c-myc and p53,and causing apoptosis of normal cells.
文摘The role of growth factors and proto-oncogene in pulmonary vascular structural remodelling is not well known.The present study examined gene expression of platelet-derived growth factor(PDGF)-A and -B chain and proto-oncogene,c-myc,in lung tissue and pulmonary artery of rats exposed to hypoxia and compared to those levels of gene expression in normal rats.Normal lungs and pulmonary artery expressed PDGF-A chain transcript of 1.7 kb and PDGF-B chain transcript of 3.5 Kb.The c-myc transcript of 2.2 kb was expressed as well. After hypoxic exposure for 7 and 14 days mRNA levels of PDGF-B chain and cmyc were elevated significantly compared with those of control rats.PDGF-A chain mRNA increased after hypoxia for 7 days,and then declined.These results suggest that activation of autocrine and/or paracrine is important in proliferation mechanism of pulmonary artery smooth muscle cells in hypoxic pulmonary hypertensive rats.
基金Supported by National Science Funds, No. 30471689
文摘AIM： To evaluate the effect of hydroxyapatite nano- particles （Nano HAP） by intravenous injection on the inhibition of implanted hepatic VX2 tumor growth in rabbits and cell p53/c-Myc protein expression. METHODS： 60 hepatic VX2 tumor-bearing rabbits was randomly divided into five groups. Nano HAP collosol 20 mglkg, 40 mg/kg, 5-FU solutions 20 mg/mL, mixed liquor of 5-FU solution 20 mg/mL and Nano HAP collosol 20 mg/kg were infused by vein, normal saline conducted as the control. The general state, weight, liver function and gross tumor volume were detected dynamically. The expression of p53 and c-Myc gene protein in tumor tissue was detected by immunohistochemistry methods. RESULTS： The growth of implanted hepatic VX2 tumors was significantly inhibited in all therapy groups, 3 wk after the injection, the tumor control rates in Nano HAP collosol groups were 25.5% and 32.5% respectively, and the gross tumor volumes were obviously less than that of control group. （24.81 ± 5.17 and 22.73 ± 4.23 vs 33.32 ± 5.26, P 〈 0.05）. The tumor control rate of 5-FU group was 43.7% （18.74 4± 4.40 vs 33.32 ± 5.26, P 〈 0.05）, but the general state of the animals after injection aggravated; and the adverse reaction in the drug combination group obviously decreased. Due to the effect of Nano HAP, the positive expression of tumor associated the mutated p53 and c-Myc in tumor tissue was decreased obviously compared with the control group. CONCLUSION： Nano HAP has evident inhibitory action on rabbit implanted hepatic VX2 tumor in vivo, which may be the result of decreasing the expression of the mutated p53 and c-myc, and drug combination can obviously decrease the adverse reaction of 5-FU.
文摘AIM: To investigate the interrelationship between H pylori and Epstein-Barr virus (EBV) infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc, Bcl-2 and Bax expression. METHODS: seventy-one gastric carcinoma tissues were assessed by polymerase chain reaction (PCR) for H pylori and in situ hybridization for EBV. c-Myc, Bcl-2 and Bax expression were detected by immunohistochemistry and single-stranded conformational polymorphism (SSCP) for p53 mutation. RESULTS: The positivity rates for H pylori and EBV were 94.4% and 8.45%, respectively. The majority of the cases displayed only the H pylori presence. All EBV positive cases were also H pylori positive. None infectious agent was observed in 5.55% of the cases. The intestinal type tumor was more frequent in the co-infected and non-infected groups. The female predominated in the non-infected group showing statistical significance (70.4% vs 29.6%, P=0.039). The Bcl-2 was only detected in the group exclusively infected by H pylori. However, c-Myc and Bax were detected in the three groups but with a low frequency in the co-infected group. Mutation of p53 was present in all groups, with the highest frequencies in the H pylori positive groups. CONCLUSION: The frequency of H pylori infection in gastric carcinomas was high. The presented data indicated that gastric carcinogenesis has different pathways depending of the presence of the two investigated infectious agents, suggesting a possible involvement of H pylori with apoptotic process. The low expression of c-Myc and Bax in the EBV-positive groups suggests that EBV may inhibit the expression of these proteins. Nevertheless, p53 mutation shows to be a relevant alteration, independent of both infectious agents.
