Knocking down of FANCI expression inhibits the biological behavior of glioma and mediates apoptosis by downregulating the Akt/Bcl2 pathway

Abstract

Abstract Purpose Previous studies have shown that FANCI has cancer susceptibility, and high expression of FANCI promotes the progression of breast cancer, ovarian cancer, and other cancers. However, the potential mechanism of action of FANCI in glioma progression is unclear. Methods To explore the role of FANCI in glioma progression, we determined the expression of FANCI in glioma patients and its relationship with prognosis through database analysis and gene chip. And then further conducted in vitro functional experiments (overexpression and knockdown) and in vivo nude mouse xenograft model experiments. Results This study found that FANCI was significantly overexpressed in glioma, positively correlated with WHO grade, and closely related to patient prognosis. In vitro functional experiments showed that inhibiting the expression of FANCI could inhibit the proliferation, migration, and invasion of glioma and promote apoptosis. At the same time, the nude mouse xenograft model also confirmed that inhibition of FANCI could inhibit glioma in vivo. In addition, the low expression of FANCI inhibited the phosphorylation of Akt and the expression of Bcl-2 by western blotting. Conclusion FANCI promotes glioma growth and may mediate apoptosis by regulating Akt/Bcl-2. This study preliminarily explored the role of FANCI in glioma growth and provided data support for further application of FANCI in clinical practice.