Interleukin-17 promotes migration and invasion of human cancer cells through upregulation of MTA1 expression

32Citations
Citations of this article
41Readers
Mendeley users who have this article in their library.

Abstract

Interleukin-17 (IL-17) has been shown to promote development of prostate, colon, skin, lung, breast, and pancreatic cancer. The purpose of this study was to determine if IL-17 regulates MTA1 expression and its biological consequences. Human cervical cancer HeLa and human prostate cancer DU-145 cell lines were used to test if IL-17 regulates metastasis associated 1 (MTA1) mRNA and protein expression using quantitative reverse transcription-polymerase chain reaction and Western blot analysis, respectively. Cell migration and invasion were studied using wound healing assays and invasion chamber assays. Thirty-four human cervical tissues were stained for IL-17 and MTA1 using immunohistochemical staining. We found that IL-17 increased MTA1 mRNA and protein expression in both cell lines. Cell migration was accelerated by IL-17, which was abolished by knockdown of MTA1 expression with small interference RNA (siRNA). Further, cell invasion was enhanced by IL-17, which was eliminated by MTA1 knockdown. Human cervical intra-epithelial neoplasia (CIN) and cervical cancer tissues had increased number of IL-17-positive cells and MTA1 expression compared to normal cervical tissues. The number of IL-17positive cells was positively correlated with MTA1 expression. These findings demonstrate that IL-17 upregulates MTA1 mRNA and protein expression to promote HeLa and DU-145 cell migration and invasion.

Cite

CITATION STYLE

APA

Guo, N., Shen, G., Zhang, Y., Moustafa, A. A., Ge, D., & You, Z. (2019). Interleukin-17 promotes migration and invasion of human cancer cells through upregulation of MTA1 expression. Frontiers in Oncology, 9(JUN). https://doi.org/10.3389/fonc.2019.00546

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free