Grifolin induces apoptosis and promotes cell cycle arrest in the A2780 human ovarian cancer cell line via inactivation of the ERK1/2 and Akt pathways.

Grifolin, a secondary metabolic product isolated from the mushroom , has been demonstrated to possess antitumor activities in a variety of malignant cells. However, the signaling pathways and the molecular mechanisms underlying the anticancer effects of the agent in human ovarian cancer remain to be elucidated. The aim of the present study was to examine the effect of grifolin treatment on the human ovarian cancer cell line, A2780. MTT and flow cytometry analysis were used to analyze the viability of A2780 cells following treatment with grifolin. Western blotting was used analyze the expression of apoptosis-associated and cell cycle arrest-associated proteins. The results of MTT assays and flow cytometry analysis revealed that grifolin suppressed cell viability, induced apoptosis and triggered cell cycle arrest. Western blotting revealed that grifolin treatment resulted in inactivation of protein kinase B (Akt) and extracellular signal-related kinase 1/2 (ERK1/2), accompanied by upregulation of Bcl-2 associated X, apoptosis regulator, cleaved-caspase-3 and cleaved-poly (ADP-ribose) polymerase, and downregulation of B cell lymphoma-2, cyclin dependent kinase 4 and cyclinD1. The results of the present study indicated that grifolin had significant anti-cancer effects on the human ovarian cancer A2780 cells, which occurred via the Akt and ERK1/2 signaling pathways to at least a certain extent. These results demonstrate the therapeutic potential of grifolin as a treatment for ovarian cancer.