Wogonin inhibitsovarian cancer by activating the AMPK-TET2-5hmC axis

Ovarian cancer is one of the most common female cancers. In the quest of effective anti-cancer agents, this study explores the effects of wogonin, a naturally occurring flavonoid, on the viability and migration of A2780 and Kuramochi ovarian cancer cell lines. Our findings demonstrate that wogonin not only impedes cancer cell growth and mobility in both in vitro and in vivo but also significantly enhances the cytotoxic efficacy of cisplatin. Mechanistic investigations reveal that wogonin suppresses genes associated with proliferation and EMT and upregulates metabolic pathways, particularly the AMPK signaling, which is crucial for increasing 5hmC levels, highlighting wogonin's role in promoting DNA demethylation through the stabilization of TET2. Our findings not only highlights the therapeutic potential of wogonin but also its preventative capability against ovarian cancer in individuals with metabolic disorders, such as diabetes, who are at increased risk for ovarian cancer. This study highlights wogonin's dual functionality in ovarian cancer treatment and prevention, emphasizing its promising prospects for future oncological applications. Overall design: we aim to investigate if wogonin can inhibit ovarian cancer growth, by affecting the DNA demethylation process.