Curcumin can suppress the growth of prostate cancer cells. - GreenMedInfo Summary
[Curcumin inhibits the expression of vascular endothelial growth factor and androgen-independent prostate cancer cell line PC-3 in vitro].
Zhonghua Nan Ke Xue. 2008 Feb;14(2):116-21. PMID: 18390174
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science&Technology, Wuhan , Hubei 430030, China. firstname.lastname@example.org
OBJECTIVE: To study the effects of curcumin on the expression of the vascular endothelial growth factor (VEGF) and androgen-independent prostate cancer cell line PC-3, and to explore its anticarcinogenic mechanism.
METHODS: PC-3 cells were treated with curcumin at the concentration of 0, 6.25, 12.5, 25 and 50 micromol/L respectively. Then the cell activity was assayed by dyed rate of Typan blue and MTT at 12, 24, 36, 48, 72 and 96 hours, the cell cycle and morphological changes observed by flow cytometry (FCM) and electronic microscopy at 24 hours, the VEGF mRNA expression measured by semi-quantitative RT-PCR, and the secreting protein levels of VEGF in the supernatants determined by enzyme-linked immunosorbent assay (ELISA).
RESULTS: The growth of PC-3 cells was suppressed obviously by curcumin in a dose- and time-dependent manner in vitro. There were significant differences in inhibition rate among different concentration and time groups (P<0.01). Furthermore, curcumin arrested the cell cycle of PC-3 cells in the G2/M phase in a dose-dependent manner (P<0.01). The percentages of apoptotic cells were significantly higher in different concentration groups than in the controls (P<0.01). Apoptosis-associated morphological changes were observed in PC-3 cells at 24 hours, and a marked decline in the expression of VEGF was noted after the exposure to different concentrations of curcumin within 24 hours.
CONCLUSION: Curcumin can suppress the growth of PC-3 cells, promote their apoptosis and arrest their cell cycle in the G2/M phase, and reduce the expression of VEGF mRNA and proteins, which may sever to explain its inhibitory effect on tumor and angiogenesis.