Sulforaphane regulates apoptosis-and proliferation‑related signaling pathways and synergizes with cisplatin to suppress human ovarian cancer.

Abstract

Ovarian cancer is currently the most life-threatening type of gynecological malignancy with limited treatment options. Therefore, improved targeted therapies are required to combat ovarian cancer across the world. Sulforaphane is found in raw cruciferous vegetables. The chemotherapeutic and anti-carcinogenic properties of sulforaphane have been demonstrated, however, the underlying mechanisms remain to be fully elucidated, particularly in ovarian cancer. In the present study, the possibility of repurposing sulforaphane as an anti-ovarian cancer agent was examined. Cell viability and colony formation assay were used to test the anticancer efficiency of sulforaphane. Then wound healing assay, migration assay, cell cycle and apoptosis assays were used to detect how the drug worked on the cells. The mechanism of sulforaphane was investigated by western blot analysis. It was found that sulforaphane effectively suppressed the progression of human ovarian cancer cell proliferation, migration and cell cycle, and promoted apoptosis. Sulforaphane inhibited multiple cancer-associated signaling pathways, including B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, cytochrome c, Caspase-3, phosphorylated AKT, phosphorylated nuclear factor-κB, P53, P27, Cyclin-D1 and cMyc, and reduced the expression levels of human epidermal growth factor receptor 2 in human ovarian cancer cells. Sulforaphane synergized with cisplatin to suppress the cancer cell proliferation and enhance ovarian cancer cell apoptosis. Xenograft experiments in vivo confirmed that sulforaphane effectively suppressed tumor growth by inhibiting ovarian cancer cell proliferation through targeting tumor-related signals. The results indicated that sulforaphane may be repurposed as an effective anti-ovarian cancer agent, with further preclinical or clinical investigations required.