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 with negative 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 cells was 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.