期刊论文详细信息
Journal of Experimental & Clinical Cancer Research
Overexpression of TMEM158 contributes to ovarian carcinogenesis
Xiaoyan Qu1  Weihong Yang1  Ning Luo1  Li Chen1  Jing Guo1  Zhongping Cheng1 
[1] Institute of Gynecological Minimally Invasive Medicine, Tongji University School of Medicine, Shanghai 200090, China
关键词: Cell adhesion;    TGF-β;    Cell invasion;    Ovarian cancer;    TMEM158;   
Others  :  1226288
DOI  :  10.1186/s13046-015-0193-y
 received in 2015-04-28, accepted in 2015-07-17,  发布年份 2015
【 摘 要 】

Background

Transmembrane protein 158 (TMEM158) is a recently identified upregulated gene during Ras-induced senescence. Its association with various cancers has been recently reported. However, the expression and biological function of TMEM158 in ovarian cancer is still unclear. This study was aimed to elucidate the roles of TMEM158 in cell proliferation, adhesion and cell invasion of ovarian cancer cells.

Methods

We analyzed TMEM158 mRNA level in ovarian cancer tissues and adjacent no-tumorous tissues by real-time PCR. We then suppressed TMEM158 expression of ovarian cancer cells by RNA interference and examined the effects of TMEM158 knockdown on cancerous transformation of ovarian cancer cells.

Results

The RNA-sequencing data of the ovarian cancer cohort from The Cancer Genome Atlas project (TCGA) and our real-time PCR data showed that TMEM158 was overexpressed in ovarian cancer. Knockdown of TMEM158 by RNA interference in ovarian cancer cells significantly inhibited cell proliferation, which may be due to the increase of G1-phase arrest. Silencing of TMEM158 also inhibited cell adhesion, cell invasion as well as tumorigenicity in nude mice. Moreover, knockdown of TMEM158 notably repressed cell adhesion via down-regulating the expression intercellular adhesion molecule1 (ICAM1) and vascular cell adhesion molecule1 (VCAM1). Transforming Growth Factor-β (TGF-β) signaling pathway was also remarkably impaired by TMEM158 silencing.

Conclusions

Our data suggests that TMEM158 may work as an oncogene for ovarian cancer and that inhibition of TMEM158 may be a therapeutic strategy for ovarian cancer.

【 授权许可】

   
2015 Cheng et al.

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