Lymphoid-specific helicase inhibits cervical cancer cells ferroptosis by promoting Nrf2 expression

Background. Cervical cancer is a major cause of morbidity and mortality in women worldwide. The underlying mechanisms of its progression are not well understood. In this study, we investigated the role of lymphoid-specific helicase (HELLS) in cervical cancer.Methods. We measured HELLS expression in cervical cancer and assessed its function using gain- and loss-of-function experiments. Cell viability was measured using the Cell Counting Kit-8 (CCK8 ) assay, and cell proliferation was analyzed using colony formation and EdU assays.Results. We found that HELLS was significantly increased in cervical cancer and that its overexpression promoted cell viability (P < 0.01) and colony formation (P < 0.001). In contrast, si-HELLS suppressed these effects. Moreover, HELLS overexpression inhibited cell death induced by the ferroptosis inducer erastin (P < 0.01). Mechanistically, we found that HELLS promoted cervical cancer proliferation by regulating nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated ferroptosis.Conclusion. Our data suggest that HELLS promotes cervical cancer proliferation by inhibiting Nrf2 expression. Therefore, HELLS knockdown may be an effective treatment for cervical cancer.

Automated summary

This study investigated the role of lymphoid-specific helicase (HELLS) in cervical cancer and found that its overexpression promotes cell proliferation and inhibits cell death. The suppression of Nrf2 expression by HELLS may contribute to cervical cancer progression. HELLS knockdown could be effective in treating cervical cancer.