Effect of 6-gingerol on proliferation and apoptosis of ovarian cancer cells by the PI3K/AKT/mTOR pathway

Background As a major contributor to mortality among gynecological malignancies, ovarian cancer highlights an urgent need for novel therapeutic approaches. Although 6-gingerol—a primary bioactive compound found in ginger—is recognized for its anticancer properties, its precise role and underlying mechanisms in ovarian cancer remain largely unexplored. Methods SKOV3 ovarian cancer cells were treated with varying concentrations of 6-gingerol, either alone or in combination with Recilisib, an activator of the PI3K signaling pathway. Cell viability was evaluated using the MTT assay, whereas apoptosis and cell cycle distribution were assessed via flow cytometry. Western blot analysis was conducted to measure protein levels of cyclin E, cyclin B, Beclin1, Atg7, and P62. Results 6-gingerol treatment led to a concentration-dependent reduction in cell viability, induced G2-M phase arrest, and promoted apoptosis. These changes were associated with elevated expression of Beclin1 and Atg7, alongside decreased levels of cyclin E, cyclin B, and P62 (p < 0.05). Notably, co-treatment with Recilisib significantly counteracted the effects of 6-gingerol on cell viability, cell cycle regulation, apoptosis, and the expression of autophagy-related proteins (p < 0.05). Conclusion These findings indicate that 6-gingerol may exert antitumor activity in ovarian cancer cells through inhibition of the PI3K/AKT/mTOR pathway, resulting inreduced cell viability, enhanced apoptosis, and increased autophagic activity. The pivotal involvement of this signaling cascade is supported by the observation that its targeted activation effectively reverses the actions of 6-gingerol. Collectively, these results support further investigation into the biological effects of 6-gingerol in ovarian cancer models.