In the article entitled“Preliminary study of the mechanism of isolinderalactone inhibiting the malignant behavior of bladder cancer”published in Current Urology 2025;19(1):49–58(DOI:10.1097/CU9.0000000000000259),th...In the article entitled“Preliminary study of the mechanism of isolinderalactone inhibiting the malignant behavior of bladder cancer”published in Current Urology 2025;19(1):49–58(DOI:10.1097/CU9.0000000000000259),the Statement of Ethics should be replaced to:“All the experimental protocols for animal studies were conducted in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.This study was approved by the laboratory animal welfare ethics committee of Yunnan University(Approval No.YNU20230653).”We apologize for this error and any inconvenience this may have caused.展开更多
Background:Bladder cancer(BLCA)is the most prevalent malignancy in the urinary tract system,while ST3GAL5 is a protein-coding gene that catalyzes the formation of ganglioside monosialodihexosylganglioside 3(GM3)syntha...Background:Bladder cancer(BLCA)is the most prevalent malignancy in the urinary tract system,while ST3GAL5 is a protein-coding gene that catalyzes the formation of ganglioside monosialodihexosylganglioside 3(GM3)synthase.GM3 synthase has been reported to significantly influence the malignant process of various cancers.However,the expression profile and functional role of ST3GAL5 specifucally in BLCA remain to be elucidated.Methods:In order to investigate the relationship between ST3GAL5 expression and malignant biological behavior and prognosis in BLCA.The mRNA expression of ST3GAL5 and clinicopathological characteristics in BLCA were firstly evaluated by public databases.Next,immunohistochemical staining was performed to analyze the protein expression of ST3GAL5 in BLCA and paracancerous tissues,as well as the expression of various types of malignant biological behavior.Subsequently,the gene set enrichment analyses(GSEA)were performed for ST3GAL5 and all correlated genes in BLCA by sorting Pearson's Correlation Coefficient.GSEA was also used to validate the pathways affected by the different expression levels of ST3GAL5 in BLCA patients.Results:The mRNA and protein expression of ST3GAL5 in BLCA were significantly higher in low-grade and non-muscle-invasive BLCA(p<0.05).The results from bioinformatics databases indicated that upregulation of ST3GAL5 have a lower grade,lower pathological stage,less susceptibility to lymphatic metastasis,and lower mortality rates.Kaplan–Meier survival analysis demonstrated that upregulation of ST3GAL5 was associated with better survival in BLCA(p<0.05).Conclusion:Upregulation of ST3GAL5 may be related to tumor suppression in BLCA,and may be a potential prognostic and therapeutic marker for BLCA.展开更多
Objective To investigate miR-183-5p targeting to forkhead box protein O1(FOXO1)and its corresponding effect on the proliferation,migration,invasion,and epithelial-mesenchymal transition(EMT)of non-small cell lung canc...Objective To investigate miR-183-5p targeting to forkhead box protein O1(FOXO1)and its corresponding effect on the proliferation,migration,invasion,and epithelial-mesenchymal transition(EMT)of non-small cell lung cancer(NSCLC)cells.Methods NSCLC tissues and adjacent normal tissues from 60 patients with NSCLC adenocarcinoma were obtained via pathological biopsy or intraoperative resection.Several cell lines were cultured in vitro,including the human normal lung epithelial cell line BEAS-2B and human NSCLC cell lines A549,SPCA-1,PC-9,and 95-D.miR-183-5p and FOXO1 mRNA expression in tissues and cells were detected by qRT-PCR;the corresponding correlations in NSCLC tissues were analyzed using the Pearson test,and the relationship between miR-183-5p expression and clinicopathological parameters was analyzed.The miR-183-5p-mediated regulation of FOXO1 was verified by bioinformatics prediction alongside double luciferase,RNA-binding protein immunoprecipitation(RIP)assay,and pull-down experiments.A549 cells were divided into control,anti-miR-NC,anti-miR-183-5p,miR-NC,miR-183-5p,miR-183-5p+pcDNA3.1,and miR-183-5p+pcDNA3.1-FOXO1 groups.Cell proliferation,invasion,migration,apoptosis,and cell cycle distribution were detected using an MTT assay,clone formation assay,Transwell assay,scratch test,and flow cytometry,respectively.The expression of EMT-related proteins in the cells was analyzed by western blotting.The effect of miR-185-3p silencing on the development of transplanted tumors was detected by analyzing tumor formation in nude mice.Results miR-183-5p expression was significantly higher in NSCLC tissues and cells than in adjacent normal tissues,whereas FOXO1 mRNA expression was significantly down-regulated.There was a significant negative correlation between miR-183-5p and FOXO1 mRNA in NSCLC tissues(P<0.05).Additionally,the expression of miR-183-5p was significantly correlated with tumor size,tumor differentiation,and tumor-node-metastasis stage in patients with NSCLC(P<0.05).miR-183-5p targeted and inhibited FOXO1 expression.Compared to the anti-miR-NC group,the cell proliferation,scratch healing rate,N-cadherin and vimentin protein expression,and the proportion of S phase cells were significantly lower in the anti-miR-183-5p group,whereas the protein expression of E-cadherin andα-catenin and the proportion of G0/G1 phase cells were significantly higher;additionally,the frequency of colony formation and invasion were significantly lower in the anti-miR-183-5p group(P<0.05).Compared to the miR-NC group,the cell proliferation,scratch healing rate,N-cadherin and vimentin protein expression,and the proportion of S phase cells in the miR-183-5p group were significantly higher,whereas the E-cadherin andα-catenin protein expression and the proportion of G0/G1 phase cells were significantly lower;furthermore,the frequency of colony formation and invasion were significantly higher in the miR-183-5p group(P<0.05).Compared with the miR-183-5p+pcDNA3.1 group,the OD value,scratch healing rate,N-cadherin and vimentin protein expression,and the proportion of S phase cells were significantly lower in the miR-183-5p+pcDNA3.1-FOXO1 group,whereas E-cadherin andα-catenin protein expression and the proportion of G0/G1 phase cells were significantly higher;additionally,the frequency of colony formation and invasion was significantly lower in the miR-183-5p+pcDNA3.1-FOXO1 group(P<0.05).Overall,silencing miR-185-3p inhibited the growth of transplanted tumors and promoted FOXO1 expression.Conclusion Overexpression of miR-183-5p can inhibit apoptosis and promote the proliferation,migration,invasion,and EMT,of NSCLC cells by down-regulating FOXO1 expression.展开更多
Background and Aims:Cell cycle checkpoint-related genes(CCCRGs)are implicated in the development and progression of hepatocellular carcinoma(HCC).However,their precise roles and underlying mechanisms remain insufficie...Background and Aims:Cell cycle checkpoint-related genes(CCCRGs)are implicated in the development and progression of hepatocellular carcinoma(HCC).However,their precise roles and underlying mechanisms remain insufficiently characterized and require further investigation.This study aimed to explore the prognostic significance of CCCRGs in HCC,and to investigate the mechanism by which they promote the progression of HCC.Methods:HCC datasets from The Cancer Genome Atlas and International Cancer Genome Consortium were analyzed to identify hub genes.A prognostic model was constructed and validated using Kaplan–Meier analysis,nomogram,calibration curves,decision curve analysis,and receiver operating characteristic analysis.Immune infiltration patterns were assessed using single sample gene set enrichment analysis,while pathway activities were evaluated via gene set variation analysis.Single-cell RNA sequencing data from GSE149614 were analyzed with Seurat and CellChat to investigate cell–cell communication.Patientderived HCC specimens were examined through immunohistological evaluation,HCC cell lines were used for in vitro functional assays,and in vivo tumor growth was assessed through animal experiments.Results:CCCRGs showed significant associations with prognosis,malignant biological behavior,and immune responses in HCC.Centromere protein(CENP)I was identified as a critical hub gene that markedly promoted HCC proliferation,metastasis,and epithelial–mesenchymal transition,while inhibiting apoptosis.Mechanistically,CENPI suppressed YAP phosphorylation,enhancing its nuclear translocation and thereby driving malignant progression.Additionally,CENPI impaired immune effector cell infiltration,likely by disrupting tumor antigen presentation and chemokine-mediated CD8+T cell chemotaxis,thereby promoting immune escape.Conclusions:This study underscores the prognostic significance of CCCRGs in HCC and identifies CENPI as a key driver of tumor progression through the Hippo pathway.Furthermore,it reveals CENPI’s role in promoting immune escape,suggesting novel therapeutic targets for HCC treatment.展开更多
文摘In the article entitled“Preliminary study of the mechanism of isolinderalactone inhibiting the malignant behavior of bladder cancer”published in Current Urology 2025;19(1):49–58(DOI:10.1097/CU9.0000000000000259),the Statement of Ethics should be replaced to:“All the experimental protocols for animal studies were conducted in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.This study was approved by the laboratory animal welfare ethics committee of Yunnan University(Approval No.YNU20230653).”We apologize for this error and any inconvenience this may have caused.
基金Doctoral Fund Project of First Affiliated Hospital,School of Medicine,Shihezi University,China,Grant/Award Number:BS202110。
文摘Background:Bladder cancer(BLCA)is the most prevalent malignancy in the urinary tract system,while ST3GAL5 is a protein-coding gene that catalyzes the formation of ganglioside monosialodihexosylganglioside 3(GM3)synthase.GM3 synthase has been reported to significantly influence the malignant process of various cancers.However,the expression profile and functional role of ST3GAL5 specifucally in BLCA remain to be elucidated.Methods:In order to investigate the relationship between ST3GAL5 expression and malignant biological behavior and prognosis in BLCA.The mRNA expression of ST3GAL5 and clinicopathological characteristics in BLCA were firstly evaluated by public databases.Next,immunohistochemical staining was performed to analyze the protein expression of ST3GAL5 in BLCA and paracancerous tissues,as well as the expression of various types of malignant biological behavior.Subsequently,the gene set enrichment analyses(GSEA)were performed for ST3GAL5 and all correlated genes in BLCA by sorting Pearson's Correlation Coefficient.GSEA was also used to validate the pathways affected by the different expression levels of ST3GAL5 in BLCA patients.Results:The mRNA and protein expression of ST3GAL5 in BLCA were significantly higher in low-grade and non-muscle-invasive BLCA(p<0.05).The results from bioinformatics databases indicated that upregulation of ST3GAL5 have a lower grade,lower pathological stage,less susceptibility to lymphatic metastasis,and lower mortality rates.Kaplan–Meier survival analysis demonstrated that upregulation of ST3GAL5 was associated with better survival in BLCA(p<0.05).Conclusion:Upregulation of ST3GAL5 may be related to tumor suppression in BLCA,and may be a potential prognostic and therapeutic marker for BLCA.
文摘Objective To investigate miR-183-5p targeting to forkhead box protein O1(FOXO1)and its corresponding effect on the proliferation,migration,invasion,and epithelial-mesenchymal transition(EMT)of non-small cell lung cancer(NSCLC)cells.Methods NSCLC tissues and adjacent normal tissues from 60 patients with NSCLC adenocarcinoma were obtained via pathological biopsy or intraoperative resection.Several cell lines were cultured in vitro,including the human normal lung epithelial cell line BEAS-2B and human NSCLC cell lines A549,SPCA-1,PC-9,and 95-D.miR-183-5p and FOXO1 mRNA expression in tissues and cells were detected by qRT-PCR;the corresponding correlations in NSCLC tissues were analyzed using the Pearson test,and the relationship between miR-183-5p expression and clinicopathological parameters was analyzed.The miR-183-5p-mediated regulation of FOXO1 was verified by bioinformatics prediction alongside double luciferase,RNA-binding protein immunoprecipitation(RIP)assay,and pull-down experiments.A549 cells were divided into control,anti-miR-NC,anti-miR-183-5p,miR-NC,miR-183-5p,miR-183-5p+pcDNA3.1,and miR-183-5p+pcDNA3.1-FOXO1 groups.Cell proliferation,invasion,migration,apoptosis,and cell cycle distribution were detected using an MTT assay,clone formation assay,Transwell assay,scratch test,and flow cytometry,respectively.The expression of EMT-related proteins in the cells was analyzed by western blotting.The effect of miR-185-3p silencing on the development of transplanted tumors was detected by analyzing tumor formation in nude mice.Results miR-183-5p expression was significantly higher in NSCLC tissues and cells than in adjacent normal tissues,whereas FOXO1 mRNA expression was significantly down-regulated.There was a significant negative correlation between miR-183-5p and FOXO1 mRNA in NSCLC tissues(P<0.05).Additionally,the expression of miR-183-5p was significantly correlated with tumor size,tumor differentiation,and tumor-node-metastasis stage in patients with NSCLC(P<0.05).miR-183-5p targeted and inhibited FOXO1 expression.Compared to the anti-miR-NC group,the cell proliferation,scratch healing rate,N-cadherin and vimentin protein expression,and the proportion of S phase cells were significantly lower in the anti-miR-183-5p group,whereas the protein expression of E-cadherin andα-catenin and the proportion of G0/G1 phase cells were significantly higher;additionally,the frequency of colony formation and invasion were significantly lower in the anti-miR-183-5p group(P<0.05).Compared to the miR-NC group,the cell proliferation,scratch healing rate,N-cadherin and vimentin protein expression,and the proportion of S phase cells in the miR-183-5p group were significantly higher,whereas the E-cadherin andα-catenin protein expression and the proportion of G0/G1 phase cells were significantly lower;furthermore,the frequency of colony formation and invasion were significantly higher in the miR-183-5p group(P<0.05).Compared with the miR-183-5p+pcDNA3.1 group,the OD value,scratch healing rate,N-cadherin and vimentin protein expression,and the proportion of S phase cells were significantly lower in the miR-183-5p+pcDNA3.1-FOXO1 group,whereas E-cadherin andα-catenin protein expression and the proportion of G0/G1 phase cells were significantly higher;additionally,the frequency of colony formation and invasion was significantly lower in the miR-183-5p+pcDNA3.1-FOXO1 group(P<0.05).Overall,silencing miR-185-3p inhibited the growth of transplanted tumors and promoted FOXO1 expression.Conclusion Overexpression of miR-183-5p can inhibit apoptosis and promote the proliferation,migration,invasion,and EMT,of NSCLC cells by down-regulating FOXO1 expression.
基金funded by the National Natural Science Foundation of China(Grant Nos.82472743 and 82300921)the Key R&D Program of Heilongjiang Province(Grant No.GZ2024023)+1 种基金the Natural Science Foundation of Heilongjiang Province(Grant No.LH2023H043)the Open Funds of the State Key Laboratory of Oncology in South China(Grant No.HN2025-02).
文摘Background and Aims:Cell cycle checkpoint-related genes(CCCRGs)are implicated in the development and progression of hepatocellular carcinoma(HCC).However,their precise roles and underlying mechanisms remain insufficiently characterized and require further investigation.This study aimed to explore the prognostic significance of CCCRGs in HCC,and to investigate the mechanism by which they promote the progression of HCC.Methods:HCC datasets from The Cancer Genome Atlas and International Cancer Genome Consortium were analyzed to identify hub genes.A prognostic model was constructed and validated using Kaplan–Meier analysis,nomogram,calibration curves,decision curve analysis,and receiver operating characteristic analysis.Immune infiltration patterns were assessed using single sample gene set enrichment analysis,while pathway activities were evaluated via gene set variation analysis.Single-cell RNA sequencing data from GSE149614 were analyzed with Seurat and CellChat to investigate cell–cell communication.Patientderived HCC specimens were examined through immunohistological evaluation,HCC cell lines were used for in vitro functional assays,and in vivo tumor growth was assessed through animal experiments.Results:CCCRGs showed significant associations with prognosis,malignant biological behavior,and immune responses in HCC.Centromere protein(CENP)I was identified as a critical hub gene that markedly promoted HCC proliferation,metastasis,and epithelial–mesenchymal transition,while inhibiting apoptosis.Mechanistically,CENPI suppressed YAP phosphorylation,enhancing its nuclear translocation and thereby driving malignant progression.Additionally,CENPI impaired immune effector cell infiltration,likely by disrupting tumor antigen presentation and chemokine-mediated CD8+T cell chemotaxis,thereby promoting immune escape.Conclusions:This study underscores the prognostic significance of CCCRGs in HCC and identifies CENPI as a key driver of tumor progression through the Hippo pathway.Furthermore,it reveals CENPI’s role in promoting immune escape,suggesting novel therapeutic targets for HCC treatment.
