Breast cancer is the most common cancer in women,and approximately 90% of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells.Epithelial-mesenchymal transition(EMT) is a vital proce...Breast cancer is the most common cancer in women,and approximately 90% of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells.Epithelial-mesenchymal transition(EMT) is a vital process for large-scale cell movement during morphogenesis at the time of embryonic development.Tumor cells usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis.Several transcription factors and signals are involved in these events.In this review,we summarize recent advances in breast cancer researches that have provided new insights in the molecular mechanisms underlying EMT regulation during breast cancer progression and metastasis.We especially focus on the molecular pathways that control EMT.展开更多
目的:研究RNA结合基序单链相互作用蛋白3(RNA-binding motif,single-stranded-interacting protein 3,RBMS3)对胃癌细胞侵袭的影响,并探讨其可能的分子作用机制。方法:首先采用实时荧光定量PCR和蛋白质印迹法检测人正常胃黏膜上皮细胞GE...目的:研究RNA结合基序单链相互作用蛋白3(RNA-binding motif,single-stranded-interacting protein 3,RBMS3)对胃癌细胞侵袭的影响,并探讨其可能的分子作用机制。方法:首先采用实时荧光定量PCR和蛋白质印迹法检测人正常胃黏膜上皮细胞GES-1以及胃癌细胞MKN-28、MKN-45、NCI-N87和SGC-7901中RBMS3的表达水平。然后采用脂质体转染法将RBMS3过表达载体[RBMS3-pcDNA3.1(+)]转染至胃癌MKN-45和SGC-7901细胞中,同时设置空白对照组和空载体转染的阴性对照组。采用实时荧光定量PCR和蛋白质印迹法验证RBMS3过表达效果后,Transwell小室法检测细胞侵袭能力的变化,实时荧光定量PCR和蛋白质印迹法检测细胞中上皮-间质转化相关蛋白以及Wnt信号通路中β-连环蛋白(β-catenin)的表达水平变化。最后,用Wnt通路激动剂氯化锂(lithium chloride,LiCl)处理RBMS3过表达的胃癌MKN-45和SGC-7901细胞后,再次采用Transwell小室法检测细胞侵袭能力的变化。结果:与正常胃黏膜细胞相比,4种胃癌细胞中RBMS3 mRNA和蛋白的表达水平均明显降低(P值均<0.05)。RBMS3过表达质粒转染后,胃癌MKN-45和SGC-7901细胞中RBMS 3基因过表达,2种细胞的侵袭能力随之明显降低(P值均<0.05)。在RBMS3过表达的胃癌MKN-45和SGC-7901细胞中,N-钙黏蛋白(N-cadherin)和β-catenin表达水平均明显降低(P值均<0.05),而E-钙黏蛋白(E-cadherin)表达水平明显升高(P值均<0.05)。用LiCl处理RBMS3过表达的MKN-45和SGC-7901细胞后,RBMS3对2种细胞侵袭的抑制作用均被部分抵消(P值均<0.05)。结论:RBMS3可能通过阻滞Wnt/β-catenin信号通路,抑制人胃癌细胞的侵袭和上皮-间质转化。展开更多
基金supported by the grants from NIH (RO1CA125454)the Susan G. Komen Foundation (KG081310)the Mary Kay Ash Foundation (to B.P. Zhou)
文摘Breast cancer is the most common cancer in women,and approximately 90% of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells.Epithelial-mesenchymal transition(EMT) is a vital process for large-scale cell movement during morphogenesis at the time of embryonic development.Tumor cells usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis.Several transcription factors and signals are involved in these events.In this review,we summarize recent advances in breast cancer researches that have provided new insights in the molecular mechanisms underlying EMT regulation during breast cancer progression and metastasis.We especially focus on the molecular pathways that control EMT.
文摘目的探讨转化生长因子β1对脑胶质瘤细胞SF767细胞侵袭能力的影响以及可能的分子机制。方法转化生长因子β1分别干预脑胶质瘤细胞SF767细胞12、24、48 h,Western blotting检测EMT和ERK/MAPK通路相关蛋白表达情况,MTT法检测和对比干预前后细胞增殖情况,体外侵袭实验观察细胞侵袭能力改变。结果 Western blotting显示E-cadherin表达下调,而Vimentin和MMP-2表达上调。在ERK/MAPK信号转导通路中,ERK表达未见变化,但P-ERK表达上调,核转录因子Zeb-1表达增强。体外增殖实验显示干预后细胞倍增时间明显缩短;体外侵袭实验显示干预后穿膜细胞明显增多,统计学显示有显著性差异(P<0.05)。结论转化生长因子β1可能通过ERK/MAPK信号转导通路诱导EMT促进脑胶质瘤细胞SF767细胞侵袭。
