Indirubin inhibits the proliferation of prostate cancer PC-3 cells.
- Author:
Yun-fei WEI
;
Jian SU
;
Zhong-lei DENG
;
Chen ZHU
;
Lin YUAN
;
Zi-jie LU
;
Qing-yi ZHU
- Publication Type:Journal Article
- MeSH: Antibiotics, Antineoplastic; administration & dosage; pharmacology; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Cell Survival; drug effects; Coloring Agents; Cyclin D1; metabolism; Dose-Response Relationship, Drug; Genes, myc; Humans; Indoles; administration & dosage; pharmacology; Male; Prostatic Neoplasms, Castration-Resistant; drug therapy; pathology; Proto-Oncogene Proteins c-myc; metabolism; Tetrazolium Salts; Thiazoles
- From: National Journal of Andrology 2015;21(9):788-791
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the antitumoral effect of indirubin on androgen-independent prostate cancer PC-3 cells and its possible mechanisms.
METHODSWe measured the inhibitory effect of indirubin on the proliferation of prostate cancer PC-3 cells using MTT assay, detected their cell cycles by flow cytometry, and determined the expressions of the cell cycle regulatory protein cyclin D1 and its related downstream gene c-myc by Western blot.
RESULTSThe viability of the PC-3 cells was significantly decreased by indirubin in a concentration-dependent manner, reduced to 52. 2% and 13. 6% at 5 and 10 µmol/L, respectively. The cell cycle of the PC-3 cells was markedly inhibited by indirubin at 5 µmol/L, with the cells remarkably increased in the G0 and G1 phases and decreased in the S and G2/M phases. Meanwhile, indirubin also inhibited the expressions of cyclin D1 and c-myc in the Wnt signaling pathway.
CONCLUSIONIndirubin can suppress the proliferation of androgen-independent prostate cancer PC-3 cells, which may be associated with its inhibitory effect on the cell cycle and Wnt signaling pathway.