Prostate cancer is one of the most often diagnosed malignancies in males and its prevalence is rising in both developed and developing countries.Androgen deprivation therapy has been used as a standard treatment appro...Prostate cancer is one of the most often diagnosed malignancies in males and its prevalence is rising in both developed and developing countries.Androgen deprivation therapy has been used as a standard treatment approach for advanced prostate cancer for more than 80 years.The primary aim of androgen deprivation therapy is to decrease circulatory androgen and block androgen signaling.Although a partly remediation is accomplished at the beginning of treatment,some cell populations become refractory to androgen deprivation therapy and continue to metastasize.Recent evidences suggest that androgen deprivation therapy may cause cadherin switching,from E-cadherin to N-cadherin,which is the hallmark of epithelial-mesenchymal transition.Diverse direct and indirect mechanisms are involved in this switching and consequently,the cadherin pool changes from E-cadherin to N-cadherin in the epithelial cells.Since E-cadherin represses invasive and migrative behaviors of the tumor cells,the loss of E-cadherin disrupts epithelial tissue structure leading to the release of tumor cells into surrounding tissues and circulation.In this study,we review the androgen deprivation therapy-dependent cadherin switching in advanced prostate cancer with emphasis on its molecular basis especially the transcriptional factors regulated through TFG-βpathway.展开更多
目的探索P120-连环蛋白(P120ctn)在口腔鳞状细胞癌(OSCC)细胞钙黏蛋白转换中的作用及其对肿瘤细胞迁移和侵袭的影响。方法采用质粒p GFP-V-RS-P120ctn sh RNA转染OSCC细胞株TSCCA,采用实时荧光定量聚合酶链反应、Western blot检测细胞中...目的探索P120-连环蛋白(P120ctn)在口腔鳞状细胞癌(OSCC)细胞钙黏蛋白转换中的作用及其对肿瘤细胞迁移和侵袭的影响。方法采用质粒p GFP-V-RS-P120ctn sh RNA转染OSCC细胞株TSCCA,采用实时荧光定量聚合酶链反应、Western blot检测细胞中P120ctn、E-钙黏蛋白(E-cad)和N-钙黏蛋白(N-cad)的m RNA和蛋白表达的变化,通过Transwell细胞侵袭及细胞迁移实验检测转染前后细胞迁移和侵袭能力的变化。结果质粒p GFP-V-RSP120ctn sh RNA转染TSCCA细胞后,P120ctn表达明显降低,E-cad的m RNA和蛋白表达水平也明显降低,而N-cad的m RNA和蛋白表达水平明显提高,细胞迁移和侵袭能力也明显提高,差异均有统计学意义(P<0.05)。结论在OSCC中P120ctn可能通过介导钙黏蛋白转换来调节肿瘤的浸润和转移过程。展开更多
文摘Prostate cancer is one of the most often diagnosed malignancies in males and its prevalence is rising in both developed and developing countries.Androgen deprivation therapy has been used as a standard treatment approach for advanced prostate cancer for more than 80 years.The primary aim of androgen deprivation therapy is to decrease circulatory androgen and block androgen signaling.Although a partly remediation is accomplished at the beginning of treatment,some cell populations become refractory to androgen deprivation therapy and continue to metastasize.Recent evidences suggest that androgen deprivation therapy may cause cadherin switching,from E-cadherin to N-cadherin,which is the hallmark of epithelial-mesenchymal transition.Diverse direct and indirect mechanisms are involved in this switching and consequently,the cadherin pool changes from E-cadherin to N-cadherin in the epithelial cells.Since E-cadherin represses invasive and migrative behaviors of the tumor cells,the loss of E-cadherin disrupts epithelial tissue structure leading to the release of tumor cells into surrounding tissues and circulation.In this study,we review the androgen deprivation therapy-dependent cadherin switching in advanced prostate cancer with emphasis on its molecular basis especially the transcriptional factors regulated through TFG-βpathway.
