Targeting Autophagy in Ovarian Cancer: The Emerging Role of Ginsenosides

Ovarian cancer, the third most prevalent gynecological malignancy, is frequently diagnosed at an advanced stage owing to its asymptomatic early progression. Despite the application of conventional therapies, clinical management remains limited by adverse effects and the development of drug resistance. Therefore, the identification of novel therapeutic targets and strategies is urgently needed. Autophagy, a tightly regulated cellular degradation process, plays a dual and context-dependent role in cancer progression and chemoresistance and has emerged as a promising therapeutic target in ovarian cancer. Ginsenosides, the major bioactive constituents of ginseng, exhibit significant anticancer activity in a variety of tumors.

A literature review was conducted to summarize current studies on autophagy regulation in ovarian cancer and the structural characteristics and pharmacological activities of ginsenosides, with particular attention to the molecular mechanisms through which ginsenosides modulate autophagy and their potential therapeutic implications in ovarian cancer.

Ginsenosides can modulate autophagy through multiple mechanisms, including activation of the AMPK/mTOR signaling pathway, induction of reactive oxygen species (ROS) accumulation, and regulation of autophagy-related genes (ATGs), ultimately contributing to tumor suppression. Moreover, ginsenosides have demonstrated notable anticancer effects in ovarian cancer, further highlighting their potential clinical value.

This review provides a comprehensive overview of current knowledge regarding autophagy regulation in ovarian cancer, summarizes the structural and pharmacological characteristics of ginsenosides, and discusses their emerging role as autophagy-targeting agents, particularly in the treatment of this malignancy. Collectively, these insights offer a new perspective for the development of autophagy-based precision therapies for ovarian cancer.