Silencing of FOXG1 confers radio-sensitivity through regulating autophagy in glioma cells

Abstract Background/Aim forkhead box G1 (FOXG1) has recently been observed in many cancers, while its effect on radio-sensitivity in glioma is still unclear. In this study, we hypothesized that FOXG1 be a major players in radio-resistance of glioma as well as the underlying mechanism.Methods Immunohistochemistry (IHC) was conducted to assess FOXG1 expression in the glioma tissues and glioma-adjacent tissues. Western Blot was applied to detect the expression of autophagy-related proteins. CCK-8 and flow cytometry assays were applied to assess proliferation and apoptosis, respectively.Results The present study demonstrated that FOXG1 was highly expressed in glioma tissues. FOXG1 silencing enhances the effect of X-ray irradiation on proliferation inhibition and apoptosis of glioma cells, while FOXG1 overexpression has the opposite effect. Interestingly, the chloroquine (CQ) of autophagy inhibitor enhanced X-ray irradiation induces proliferation inhibition and apoptosis in glioma cells.Conclusions The present study suggests that FOXG1 is a pivotal molecule for circumventing radiation-induced cell death in malignant glioma cells through the regulation of autophagy and provide a target for the treatment of human brain glioma.