Open AccessKnockdown of Mediator Complex Subunit 19 Suppresses the Growth and Invasion of Prostate Cancer Cells
Author(s) -
Shengqiang Yu,
Yanwei Wang,
Hualei Yuan,
Hongwei Zhao,
Wei Lv,
Jian Chen,
Fang Wan,
Dongfu Liu,
Zhenli Gao,
Jitao Wu
Publication year - 2017
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0171134
Subject(s) - gene knockdown , lncap , vimentin , prostate cancer , epithelial–mesenchymal transition , cancer research , cell growth , metastasis , cell cycle , cell migration , cell , cancer , biology , pathology , chemistry , cell culture , medicine , immunohistochemistry , genetics
Prostate cancer (PCa) is one of the most common cancers in elderly men. Mediator Complex Subunit 19 (Med19) is overexpressed and plays promotional roles in many cancers. However, the roles of Med19 in PCa are still obscure. In this study, by using immunohistochemical staining, we found higher expression level of Med19 in PCa tissues than in adjacent benign prostate tissues. We then knocked down the Med19 expression in PCa cell lines LNCaP and PC3 by using lentivirus siRNA. Cell proliferation, anchor-independent growth, migration, and invasion were suppressed in Med19 knockdown PCa cells. In nude mice xenograft model, we found that Med19 knockdown PCa cells formed smaller tumors with lower proliferation index than did control cells. In the mechanism study, we found that Med19 could regulate genes involved in cell proliferation, cell cycle, and epithelial-mesenchymal transition, including P27, pAKT, pPI3K, IGF1R, E-Cadherin, N-Cadherin, Vimentin, ZEB2, Snail-1 and Snail-2. Targeting Med19 in PCa cells could inhibit the PCa growth and metastasis, and might be a therapeutic option for PCa in the future.