Molecular mechanism of metastasis in breast adenocarcinoma regulated by xCT
10.7644/j.issn.1674-9960.2015.05.004
- VernacularTitle:xCT调节乳腺癌细胞转移的作用机制研究
- Author:
Xueting ZHENG
;
Fei ZHAO
;
Rui ZHAO
;
Liping ZHAO
;
Haixuan QIAO
- Publication Type:Journal Article
- Keywords:
breast cancer cell MDA-MB-231;
autophagy;
EMT;
SASP;
RNAi
- From:
Military Medical Sciences
2015;(5):334-338,363
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of xCT on tumor metastasis in breast cancer cell MDA-MB-231. Methods Wound scratch assay and Transwell assay were performed to evaluate the effect of disruption and knockdown of xCT on cell migration and cell invasion in breast cancer cell MDA-MB-231 .Western Blot and RT-PCR were used to detect the expression levels of autophagy and EMT related markers in breast cancer cell MDA-MB-231 after treatment with sulfasalazine (SASP), an inhibitor of xCT activity and SLC7A11-RNAi.Results Both the scratch assay and the transwell migration assay showed that inhibition of xCT reduced the motility of MDA-MB-231 .The expression level of autophagy related protein LC3-Ⅱ/LC3-Ⅰwas elevated, the protein level of transcription factor Snail was down-regulated, while the mRNA level of Snail did not change in xCT inhibited MDA-MB-231 cells compared with MDA-MB-231 cells.Epithelial marker E-cadherin was up-regulated but mesenchymal marker Vimentin was down-regulated when xCT was deficient.Con-clusion Our current studies show that xCT is an endogenous regulator of tumor growth and metastasis in MDA -MB-231 and the expression level of xCT determines the phenotypes of MDA-MB-231 cells in invasion and migration in vitro.Inhibition of xCT can activate autophagy , induce the degradation of Snail ,and attenuate the EMT process in highly metastatic MDA-MB-231 cells.
