Inhibition of epithelial to mesenchymal transition in metastatic breast carcinoma cells by c-Src suppression

被引:51
作者
Liu, Xiang [1 ]
Feng, Renqing [1 ]
机构
[1] Peking Univ, Coll Life Sci, Beijing 100871, Peoples R China
基金
中国国家自然科学基金; 北京市自然科学基金;
关键词
c-Src; PP2; siRNA; breast carcinoma; epithelial to mesenchymal transition; FOCAL ADHESION KINASE; TRANSCRIPTION FACTORS; CANCER-CELLS; E-CADHERIN; TGF-BETA; ACTIVATION; EXPRESSION; SNAIL; TWIST; SLUG;
D O I
10.1093/abbs/gmq043
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aberrant activation of c-Src regulates multiple functions during tumor progression. This study was conducted to investigate the role of c-Src suppression in epithelial to mesenchymal transition (EMT) process in human breast carcinoma cells. c-Src suppression by PP2 (a Src-family kinase inhibitor) or small interfering RNA (siRNA) was carried out in MCF-7 and MDA-MB-231 cells. Cell migration was analyzed by wound-healing assay. The transcription and protein levels of EMT markers and transcription factors were evaluated by reverse transcription-PCR and Western blot analysis, respectively. The changed cell morphology was photographed by light microscope. c-Src suppression by PP2 or siRNA reversed the mesenchymal-like phenotype in MDA-MB-231 cells. E-cadherin was upregulated in MCF-7 and MDA-MB-231 cells after c-Src suppression, whereas vimentin was downregulated in MDA-MB-231 cells. Slug and SIP1 were downregulated after c-Src suppression in MCF-7 and MDA-MB-231 cells, whereas Twist was unchanged. These results suggest that c-Src suppression by PP2 or siRNA may inhibit EMT through regulation of different transcription factors in breast carcinoma cells that have different metastatic potential.
引用
收藏
页码:496 / 501
页数:6
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