Abstract
Ovarian cancer is a leading gynecological malignancy associated with high mortality. Hedgehog signaling has been found to be important for cell proliferation and tumor growth for multiple cancers, including ovarian cancer. The present study showed that the drug cyclopamine, which blocks the hedgehog signaling pathway, could reduce cancer cell growth and proliferation and induce cell apoptosis. In addition, the silencing of the glioma-associated oncogene (Gli)3, a downstream component of the hedgehog signaling pathway, could further enhance the antitumor effects of cyclopamine. Our results suggest that Gli3 may act as resistance to cyclopamine's effect on tumor growth. The combined treatment of cyclopamine application and Gli3 silencing therapy, therefore, may provide novel directions for clinical management of ovarian cancer.