Emodin induces apoptosis in human prostate cancer cell LNCaP.
- Author:
Chun-Xiao YU
1
;
Xiao-Qian ZHANG
;
Lu-Dong KANG
;
Peng-Ju ZHANG
;
Wei-Wen CHEN
;
Wen-Wen LIU
;
Qing-Wei LIU
;
Jian-Ye ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Adenocarcinoma; metabolism; pathology; Apoptosis; drug effects; Caspase 3; metabolism; Caspase 9; metabolism; Cell Line, Tumor; Cell Proliferation; drug effects; Cyclin-Dependent Kinase Inhibitor p21; metabolism; Emodin; pharmacology; Humans; Male; Prostate-Specific Antigen; metabolism; Prostatic Neoplasms; metabolism; pathology; Protein Kinase Inhibitors; pharmacology; Proto-Oncogene Proteins c-bcl-2; metabolism; Receptors, Androgen; metabolism; Tumor Suppressor Protein p53; metabolism; bcl-2-Associated X Protein; metabolism
- From: Asian Journal of Andrology 2008;10(4):625-634
- CountryChina
- Language:English
-
Abstract:
AIMTo elucidate effects and mechanisms of emodin in prostate cancer cells.
METHODSViability of emodin-treated LNCaP cells and PC-3 cells was measured by MTT assay. Following emodin treatments, DNA fragmentation was assayed by agarose gel electrophoresis. Apoptosis rate and the expression of Fas and FasL were assayed by flow cytometric analysis. The mRNA expression levels of androgen receptor (AR), prostate-specific antigen (PSA), p53, p21, Bcl-2, Bax, caspase-3, -8, -9 and Fas were detected by RT-PCR, and the protein expression levels of AR, p53 and p21 were detected by Western blot analysis.
RESULTSIn contrast to PC-3, emodin caused a marked increase in apoptosis and a decrease in cell proliferation in LNCaP cells. The expression of AR and PSA was decreased and the expression of p53 and p21 was increased as the emodin concentrations were increased. In the same time, emodin induced apoptosis of LNCaP cells through the upregulation of caspase-3 and -9, as well as the increase of Bax /Bcl-2 ratio. However, it did not involve modulation of Fas or caspase-8 protein expression.
CONCLUSIONIn prostate cancer cell line, LNCaP, emodin inhibites the proliferation by AR and p53-p21 pathways, and induces apoptosis via the mitochondrial pathway.
