The role of TRPC6 in HGF-induced cell proliferation of human prostate cancer DU145 and PC3 cells

Hepatocyte growth factor （HGF） is a glycoprotein that induces prostate cancer cell proliferation, migration and invasion. The activation of transient receptor potential canonical 6 （TRPC6） channels is considered important in promoting prostate cancer cell proliferation. In this study, we assessed th...

Full description

Saved in:
Bibliographic Details
Published in:Asian journal of andrology 2010-11, Vol.12 (6), p.841-852
Main Authors: Wang, Yong, Yue, Dan, Li, Kai, Liu, Yi-Li, Ren, Chang-Shan, Wang, Ping
Format: Article
Language:English
Subjects:
AG公司
Apoptosis - drug effects
Calcium - metabolism
Cell Cycle - drug effects
Cell Line, Tumor
Cell Proliferation - drug effects
Hepatocyte Growth Factor - physiology
Humans
Male
Original
Prostatic Neoplasms - genetics
TRPC Cation Channels - physiology
TRPC6 Cation Channel
Up-Regulation
Western印迹
全细胞膜片钳
前列腺癌细胞
细胞增殖
肝细胞生长因子
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Hepatocyte growth factor （HGF） is a glycoprotein that induces prostate cancer cell proliferation, migration and invasion. The activation of transient receptor potential canonical 6 （TRPC6） channels is considered important in promoting prostate cancer cell proliferation. In this study, we assessed the role of endogenous TRPC6 channels in the HGF-induced cell proliferation of prostate cancer. Reverse transcription-PCR and Western blotting were used to investigate TRPC6 expression. Electrophysiological techniques （whole-cell patch clamp configuration） and Ca^2＋ imaging analysis were used to investigate the channel activity in cells. The effects of TRPC6 channels on cell cycle progression, cell apoptosis and cell growth were also examined. TRPC6 and c-MET were expressed in DU145 and PC3 cells. In addition, functional TRPC6 channels were present in DU145 and PC3 cells, and TRPC6 knockdown suppressed TRPC-Iike currents evoked by oleoyl-2-acetyl-sn-glycerol （OAG）. Inhibition of TRPC6 channels in DU145 and PC3 cells abolished OAG- and HGF-induced Ca^2＋ entry. Furthermore, inhibition of TRPC6 channels arrested DU145 and PC3 cells at the G2/M phase and suppressed HGF-induced cell proliferation. Collectively, our results indicate that TRPC6 has an important role in HGF-induced DU145 and PC3 cell proliferation.
ISSN:1008-682X
1745-7262
DOI:10.1038/aja.2010.85