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Farnesoid X receptor inhibits LNcaP cell proliferation via the upregulation of PTEN
Author(s) -
Jun Liu,
Shijun Tong,
Xiang Wang,
Lianxi Qu
Publication year - 2014
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2014.1894
Subject(s) - lncap , pten , prostate cancer , farnesoid x receptor , cancer research , oncogene , cell growth , cell cycle , biology , downregulation and upregulation , cancer , nuclear receptor , tumor suppressor gene , androgen receptor , medicine , carcinogenesis , pi3k/akt/mtor pathway , signal transduction , microbiology and biotechnology , gene , transcription factor , biochemistry
Prostate cancer is a form of cancer that develops in the prostate, a gland in the male reproductive system. In the present study, the activation of the farnesoid X receptor (FXR), a member of the nuclear receptor superfamily, was demonstrated to inhibit cell proliferation in LNcaP cells. Using clinical samples, mRNA and protein levels of FXR were found to be significantly decreased by quantitative PCR and western blot analysis in prostate cancer tissues. In vitro studies identified further that activation or overexpression of FXR suppressed prostate cancer cell proliferation as measured by BrdU incorporation assays. At the molecular level, the results further revealed that the expression of the tumor suppressor gene, PTEN, was upregulated by FXR activation. Therefore, the observations indicated that FXR functions as a tumor suppressor in prostate cancer, which may provide a novel method for molecular targeting cancer treatment.

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