Down-regulated BNC1 promotes glioma by inhibiting ferroptosis via TCF21/PI3K signaling pathway BNC1TCF21PI3K

Abstract

We elucidate the role of the BNC1 gene in glioma and its potential mechanism. The expression levels of BNC1 in patients with glioma or corresponding cell lines were down-regulated. High BNC1 expression increased survival rate in patients with glioma. BNC1 gene reduced cell proliferation, and enhanced ferroptosis of glioma cells through the induction of TCF21/PI3K signaling pathway. Meanwhile, BNC1 gene could decline tumor proliferation in mice model of glioma. The ferroptosis inhibitor alleviated the impact of BNC1 on glioma ferroptosis, while the ferroptosis agonist weakened the effect of BNC1 on glioma ferroptosis. SiTCF21 also declined the effects of BNC1 on ferroptosis of glioma. The enhanced expression of TCF21 also inhibited the effect of BNC1 on ferroptosis of glioma. BNC1 protein interlinked with TCF21 protein, and bioluminescence imaging demonstrated that BNC1 enhanced TCF21 expression in the brain tissue of the mouse model of glioma. In conclusion, BNC1 reduced cell proliferation, and increased ferroptosis of glioma cells by TCF21/PI3K signaling pathway, may be a feasible strategy to treat glioma.

Keywords: BNC1; Ferroptosis; Glioma; PI3K; TCF21.