Ginsenoside Rg1 triggers ferroptosis to inhibit hepatocellular carcinoma via SLC7A11 downregulation

Ginsenoside Rg1 (Rg1) has been reported to exert its adjunctive antitumor efficacy in cancer therapy, including hepatocellular carcinoma (HCC). Here, our study revealed the role of Rg1 on HCC involving ferroptosis. Functionally, Rg1 significantly inhibited the proliferation and migration ability of HCC cells, demonstrating its anti-HCC effect. In addition, Rg1 could induce the ferroptosis-related characteristics of HCC, thereby triggering ferroptosis. Mechanistically, SLC7A11 was identified as a potential downstream mediator of Rg1, and further studies are required to validate its functional role, and Rg1 inhibited the expression of SLC7A11. This downregulation of SLC7A11 by Rg1 recovered the ferroptosis sensitivity, thereby activating ferroptosis and contributing to HCC treatment. In conclusion, our findings unveil a link between Rg1 and ferroptosis, supporting a therapeutic strategy to overcome HCC by targeting ferroptosis.