HELLS inhibits cervical cancer cells ferroptosis by promoting Nrf2 expression

Cervical cancer is the leading cause of morbidity and mortality in women throughout the world, However, the underlying mechanism of cervical cancer progression is still unclear. In the current study, we found that lymphoid-specific helicase (HELLS) was significantly increased in cervical cancer. The function of HELLS was assessed by gain- and loss-function experiments. Functionally, the cell viability was assessed by CCK8 and cell proliferation was analyzed by colony formation assay. We found that HELLS overexpression significantly promoted cell viability and colony formation of cervical cancer cell, whereas HELLS inhibition suppressed these effect. Moreover, MDA and ROS induced by ferroptosis inducers erastin were restored by HELLS-OE. Mechanically, we confirm that HELLS promote cervical cancer proliferation by regulating Nrf2-mediated ferroptosis. In conclusion, our data suggest HELLS promote cervical cancer proliferation by inhibiting Nrf2 expression, and HELLS knockdown might be an effective treatment for cervical cancer.