Anti-prostate cancer effect of carvacrol via MAPK signaling pathway / 第二军医大学学报

ABSTRACT

Objective To investigate the effects of carvacrol on proliferation, apoptosis and invasion of human prostate cancer cells in vitro, and to explore the role of mitogen-activated protein kinase (MAPK) signaling pathway in the related mechanism. Methods Prostate cancer cells DU145 were treated with (carvacrol group) or without (negative control group) 80 μmol/L carvacrol for 24 or 48 hours. CCK-8 assay and cell growth curve were used to detect the proliferation of DU145 cells on day 0, 1, 2, 3, 4 and 5. Cell apoptosis and invasion were assessed by FACS method and transwell assay, respetively. RT-PCR and Western blotting analysis were used to detect the expression of matrix metalloproteinase 9 (MMP-9) and its inhibitor TIMP-1. Expressions of poly(ADP)-ribose polymerase (PARP), caspase-9, and activation of extracellular signal-regulated kinase (ERK) and p38 were also detected by Western blotting analysis. Results Compared withnegative control group , cell viability was inhibited in the carvacrol group and cell proliferation was decreased significantly on the third day of treatment(P< 0. 05, P<0. 01). Apoptosis rate of DU145 cells was significantly increased (P<0. 05) and the invasion capability of DU145 cellswas significantly decreased in the carvacrol group (P<0. 01). Expressions of TIMP-1 and caspase-9 were increased in the carvacrol group, with fragmented PRAP , activated p38 signaling pathway, and inhibited MMP-2 activity of ERK signaling pathway. Conclusion Carvacrol can inhibit cell growth, invasion and induce apoptosis of DU145 cells, which involves MAPK signaling pathway.