Abstract

Chunyan Wang^3,†,

Zhongmei Zhou⁴,

Ceshi Chen⁴,

Rong Liu^4,* and

Dianhua Wang^1,*

²Department of Neurology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, China

³Department of Pathology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, China

⁴Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China

^† These authors contributed equally to this work.

Abstract  The prostate transmembrane protein, androgen-induced 1 (PMEPA1) has been previously shown to promote solid malignancies in a variety of cancers, but the role and mechanisms of PMEPA1 in breast cancer has not been fully addressed. Here, we found that PMEPA1 was upregulated in breast cancer cell lines as well as in a set of clinical invasive breast ductal carcinomas. Interestingly, depletion of PMEPA1 decreased breast cancer stem cell (CSC)-enriched populations, while ectopic overexpression of PMEPA1 increased breast CSC-enriched populations. Furthermore, transforming growth factor-β (TGF-β) treatment was also found to upregulate PMEPA1 expression and the CSC-enriched populations in triple-negative breast cancer cell lines. TGF-β-induced PMEPA1 expression partially contributed to TGF-β-induced breast CSC maintenance. These findings suggest that TGF-β-PMEPA1 axis might provide new diagnosis and therapeutic targets for breast cancer treatment.

Keywords   PMEPA1; TGF-β; cancer stem cell

Received   2015-8-1　　

Accepted  2015-9-21

Funding  This study was supported by the grants from the National Natural Science Foundation of China (Nos. 81272930, 81322038, 31260208, 81460401, and U1132605), Strategic Priority Research Program of the Chinese Academy of Sciences, Stem Cell and Regenerative Me

* Correspondence address  Tel: +86-871-65324888; Fax: +86-871-65336015; E-mail: [email protected] (D.W.)/Tel: +86-871-5181945; Fax: +86-871-65181945; E-mail: [email protected] (R.L.)