Objective To screen miRNA profiles of malignantly transformed human bronchial epithelial cells, 16HBE-T, induced by anti-benzo[a]pyrene-trans-7,8-diol-9,10-epoxide （anti-BPDE）, and to analyze putative miR-10a target...Objective To screen miRNA profiles of malignantly transformed human bronchial epithelial cells, 16HBE-T, induced by anti-benzo[a]pyrene-trans-7,8-diol-9,10-epoxide （anti-BPDE）, and to analyze putative miR-10a targets in 16HBE-T. Methods A novel microarray platform was employed to screen miRNA profiles of 16HBE-T cells transformed by anti-BPDE. Microarray data for miR-10a and miR-320 were validated using quantitative real time polymerase chain reaction （QRT-PCR）. The expression of a putative target for miR-10a, HOXA1, was analyzed by reverse transcription polymerase chain reaction （RT-PCR） and QRT-PCR. Results In comparison with the vehicle-treated cells （16HBE-N）, 16HBE-T exhibited differential expression of 54 miRNAs, in which, 45 were over-expressed and 9 were down-regulated. The five most highly expressed miRNAs were miR-494, miR-320, miR-498, miR-129, and miR-106a. The lowest expressed miRNAs were miR-10a, miR-493-5p, and miR-363＊. Three members of miR-17-92 cluster, miR-17-5p, miR-20a, and miR-92, showed significantly higher abundance in 16BHE-T as miR-21, miR-141, miR-27a, miR-27b, miR-16 and miRNAs of the let-7 family. The putative target for miR-10a, HOXA1 mRNA was up-regulated 3-9-fold in 16HBE-T, as compared with 16HBE-N. Conclusion The findings of the study provide information on differentially expressed miRNA in malignant 16HBE-T, and also suggest a potential role of these miRNAs in cell transformation induced by anti-BPDE. HOXA1 is similarly up-regulated, suggesting that miR-10a is associated with the process of HOXA 1-mediated transformation.展开更多
Objective To study the alterations of FHIT gene and P16 gene in malignant transformed human bronchial epithelial cells induced by crystalline nickel sulfide using an immortal human bronchial epithelial cell line, and ...Objective To study the alterations of FHIT gene and P16 gene in malignant transformed human bronchial epithelial cells induced by crystalline nickel sulfide using an immortal human bronchial epithelial cell line, and to explore the molecular mechanism of nickel carcinogenesis. Methods 16HBE cells were treated 6 times with different concentrations of NiS in vitro, and the degree of malignant transformation was determined by assaying the anchorage-independent growth and tumorigenicity. Malignant transformed cells and tumorigenic cells were examined for alterations of FHIT gene and P16 gene using RT-PCR, DNA sequencing, silver staining PCR-SSCP and Western blotting. Results NiS-treated cells exhibited overlapping growth. Compared wkh that of negative control cells, soft agar colony formation efficiency of NiS-treated cells showed significant increases （P〈0.01） and dose-dependent effects. NiS-treated cells could form tumors in nude mice, and a squamous cell carcinoma was confirmed by histopathological examination. No mutation of exon 2 and exons 2-3, no abnormal expression in pl6 gene and mutation of FHIT exons 5-8 and exons 1-4 or exons 5-9 were observed in transformed cells and tumorigenic cells. However, aberrant transcripts or loss of expression of the FHIT gene and Fhit protein was observed in transformed cells and tumorigenic cells. One of the aberrant transcripts in the FHIT gene was confirmed to have a deletion of exon 6, exon 7, exon 8, and an insertion of a 36 bp sequence replacing exon 6-8. Conclusions The FHIT gene rather than the P16 gene, plays a definite role in nickel carcinogenesis. Alterations of the FHIT gene induced by crystalline NiS may be a molecular event associated with carcinogen, chromosome fragile site instability and cell malignant transformation. FHIT may be an important target gene activated by nickel and other exotic carcinogens.展开更多
A new mutant human papillomavirus type 16 E7 gene, termed HPV16 HBE7, was isolated from cervical carcinoma biopsy samples from patients in an area with high incidence of cervical cancer (Hubei province, China). A prev...A new mutant human papillomavirus type 16 E7 gene, termed HPV16 HBE7, was isolated from cervical carcinoma biopsy samples from patients in an area with high incidence of cervical cancer (Hubei province, China). A previous study showed that the HPV16 HBE7 protein was primarily cytoplasmic while wild-type HPV16 E7 protein, termed HPV16 WE7, was concentrated in the nucleus. With the aim of studying the biological functions of HPV16 HBE7, the transforming potential of HPV16 HBE7 in NIH/3T3 cells was detected through observation of cell morphology, cell proliferation assay and anchorage-independent growth assay. The effect of HPV16 HBE7 on cell cycle was examined by flow cytometry. Dual-luciferase reporter assay and RT-PCR were used to investigate the influence of HPV16 HBE7 protein on the expression of regulation factors associated with G1/S checkpoint. The results showed that HPV16 HBE7 protein, as well as HPV16 WE7 protein, held transformation activity. NIH/3T3 cells expressing HPV16 HBE7 could easily transition from G1 phase into S phase and expressed high level of cyclin A and cdc25A. These results indicated HPV16 mutant E7 protein, located in the cytoplasm, induces oncogenic transformation of NIH/3T3 cells via up-regulation of cyclin A and cdc25A.展开更多
Based on the nucleation and growth theory together with the influence of deformation on driving force and nucleation site,a numerical model was developed for predicting deformation-induced transformation(DIT).The nume...Based on the nucleation and growth theory together with the influence of deformation on driving force and nucleation site,a numerical model was developed for predicting deformation-induced transformation(DIT).The numerical results of DIT of 16 MnNb steel was presented and compared with the experimental ones.The calculated results are in agood agreement with the experimental ones,and the best calculated result is obtained when the constantα=0.25 for steel 16 MnNb.展开更多
In this paper, efficient one-dimensional (1-D) fast integer transform algorithms of the DCT matrix for the H.265 stan-dard is proposed. Based on the symmetric property of the integer transform matrix and the matrix op...In this paper, efficient one-dimensional (1-D) fast integer transform algorithms of the DCT matrix for the H.265 stan-dard is proposed. Based on the symmetric property of the integer transform matrix and the matrix operations, which denote the row/column permutations and the matrix decompositions, along with using the dyadic symmetry modification on the standard matrix, the efficient fast 1-D integer transform algorithms are developed. Therefore, the computational complexities of the proposed fast integer transform are smaller than those of the direct method. In addition to computational complexity reduction one of the proposed algorithms provides transformation quality improvement, while the other provides more computational complexity reduction while maintaining almost the same transformation quality. With lower complexity and better transformation quality, the first proposed fast algorithm is suitable to accelerate the quality-demanding video coding computations. On the other hand, with the significant lower complexity, the second proposed fast algorithm is suitable to accelerate the video coding computations.展开更多
基金supported by the National Natural Science Foundation of China(No.30571546,30771780)the Scientific Research Foundation of the State Education Ministry for Returned Overseas Chinese Scholars(2007-24)+1 种基金the Natural Science Foundation of Guangdong Province(No.07117550)the Natural Science Key Program of Higher Education Institutions of Guangdong Province,China(No.06Z021).
文摘Objective To screen miRNA profiles of malignantly transformed human bronchial epithelial cells, 16HBE-T, induced by anti-benzo[a]pyrene-trans-7,8-diol-9,10-epoxide （anti-BPDE）, and to analyze putative miR-10a targets in 16HBE-T. Methods A novel microarray platform was employed to screen miRNA profiles of 16HBE-T cells transformed by anti-BPDE. Microarray data for miR-10a and miR-320 were validated using quantitative real time polymerase chain reaction （QRT-PCR）. The expression of a putative target for miR-10a, HOXA1, was analyzed by reverse transcription polymerase chain reaction （RT-PCR） and QRT-PCR. Results In comparison with the vehicle-treated cells （16HBE-N）, 16HBE-T exhibited differential expression of 54 miRNAs, in which, 45 were over-expressed and 9 were down-regulated. The five most highly expressed miRNAs were miR-494, miR-320, miR-498, miR-129, and miR-106a. The lowest expressed miRNAs were miR-10a, miR-493-5p, and miR-363＊. Three members of miR-17-92 cluster, miR-17-5p, miR-20a, and miR-92, showed significantly higher abundance in 16BHE-T as miR-21, miR-141, miR-27a, miR-27b, miR-16 and miRNAs of the let-7 family. The putative target for miR-10a, HOXA1 mRNA was up-regulated 3-9-fold in 16HBE-T, as compared with 16HBE-N. Conclusion The findings of the study provide information on differentially expressed miRNA in malignant 16HBE-T, and also suggest a potential role of these miRNAs in cell transformation induced by anti-BPDE. HOXA1 is similarly up-regulated, suggesting that miR-10a is associated with the process of HOXA 1-mediated transformation.
基金This work was supported by a grant (No. 39170651 and 30200235) from National Natural Science Foundation of China.
文摘Objective To study the alterations of FHIT gene and P16 gene in malignant transformed human bronchial epithelial cells induced by crystalline nickel sulfide using an immortal human bronchial epithelial cell line, and to explore the molecular mechanism of nickel carcinogenesis. Methods 16HBE cells were treated 6 times with different concentrations of NiS in vitro, and the degree of malignant transformation was determined by assaying the anchorage-independent growth and tumorigenicity. Malignant transformed cells and tumorigenic cells were examined for alterations of FHIT gene and P16 gene using RT-PCR, DNA sequencing, silver staining PCR-SSCP and Western blotting. Results NiS-treated cells exhibited overlapping growth. Compared wkh that of negative control cells, soft agar colony formation efficiency of NiS-treated cells showed significant increases （P〈0.01） and dose-dependent effects. NiS-treated cells could form tumors in nude mice, and a squamous cell carcinoma was confirmed by histopathological examination. No mutation of exon 2 and exons 2-3, no abnormal expression in pl6 gene and mutation of FHIT exons 5-8 and exons 1-4 or exons 5-9 were observed in transformed cells and tumorigenic cells. However, aberrant transcripts or loss of expression of the FHIT gene and Fhit protein was observed in transformed cells and tumorigenic cells. One of the aberrant transcripts in the FHIT gene was confirmed to have a deletion of exon 6, exon 7, exon 8, and an insertion of a 36 bp sequence replacing exon 6-8. Conclusions The FHIT gene rather than the P16 gene, plays a definite role in nickel carcinogenesis. Alterations of the FHIT gene induced by crystalline NiS may be a molecular event associated with carcinogen, chromosome fragile site instability and cell malignant transformation. FHIT may be an important target gene activated by nickel and other exotic carcinogens.
基金National Natural Science Foundation of China (Grant No.30571955 and 30772308)
文摘A new mutant human papillomavirus type 16 E7 gene, termed HPV16 HBE7, was isolated from cervical carcinoma biopsy samples from patients in an area with high incidence of cervical cancer (Hubei province, China). A previous study showed that the HPV16 HBE7 protein was primarily cytoplasmic while wild-type HPV16 E7 protein, termed HPV16 WE7, was concentrated in the nucleus. With the aim of studying the biological functions of HPV16 HBE7, the transforming potential of HPV16 HBE7 in NIH/3T3 cells was detected through observation of cell morphology, cell proliferation assay and anchorage-independent growth assay. The effect of HPV16 HBE7 on cell cycle was examined by flow cytometry. Dual-luciferase reporter assay and RT-PCR were used to investigate the influence of HPV16 HBE7 protein on the expression of regulation factors associated with G1/S checkpoint. The results showed that HPV16 HBE7 protein, as well as HPV16 WE7 protein, held transformation activity. NIH/3T3 cells expressing HPV16 HBE7 could easily transition from G1 phase into S phase and expressed high level of cyclin A and cdc25A. These results indicated HPV16 mutant E7 protein, located in the cytoplasm, induces oncogenic transformation of NIH/3T3 cells via up-regulation of cyclin A and cdc25A.
文摘Based on the nucleation and growth theory together with the influence of deformation on driving force and nucleation site,a numerical model was developed for predicting deformation-induced transformation(DIT).The numerical results of DIT of 16 MnNb steel was presented and compared with the experimental ones.The calculated results are in agood agreement with the experimental ones,and the best calculated result is obtained when the constantα=0.25 for steel 16 MnNb.
文摘In this paper, efficient one-dimensional (1-D) fast integer transform algorithms of the DCT matrix for the H.265 stan-dard is proposed. Based on the symmetric property of the integer transform matrix and the matrix operations, which denote the row/column permutations and the matrix decompositions, along with using the dyadic symmetry modification on the standard matrix, the efficient fast 1-D integer transform algorithms are developed. Therefore, the computational complexities of the proposed fast integer transform are smaller than those of the direct method. In addition to computational complexity reduction one of the proposed algorithms provides transformation quality improvement, while the other provides more computational complexity reduction while maintaining almost the same transformation quality. With lower complexity and better transformation quality, the first proposed fast algorithm is suitable to accelerate the quality-demanding video coding computations. On the other hand, with the significant lower complexity, the second proposed fast algorithm is suitable to accelerate the video coding computations.
