Novel Pathogenic, Biomarker and Therapeutic Potentials of Foxm1 in Glioma

Abstract

Gliomas embody entirely prime brain tumors of glial cell or neuroepithelial derivation. Glioma is still one of the lethal human cancers notwithstanding contemporary innovations in both diagnostic techniques and therapeutic schemes. Also, glioma carries the lowest survival rate as compare to other cancers 5 years after definitive diagnosis. FoxM1 was initially identified as HFH-11, WIN, MPP2, as well as Trident. It’s an evolutionary well-maintained, with common winged helix DNA-binding domain. FoxM1 actively participates in gliomagenesis via several pathways like, FoxM1/MELK/EZH2 signaling, FoxM1/BMI-1/Ink4a/Arf/Ink4b signaling, FoxM1/IPO7/Hh signaling as well as FoxM1/PLAGL2/Wnt/β-catenin signaling. FoxM1 also augments’ the stimulation of Akt as well as secretion of survivin, cyclin E, and cyclin D1. Furthermore, FoxG1 contributes to glioma invasiveness via MMPs especially MMP-4 and MMP-9. Nevertheless, FoxM1 contributes to glioma angiogenesis via VEGF and transcription stimulators like HIF-1 and STAT3 have been implicated as VEGF facilitators. FoxM1 has also proven to a promising diagnostic and prognostic biomarker in glioma. Moreover, FoxM1 has therapeutic potential in glioma either alone or in combination with other agents. This review therefore focuses on the novel pathogenic, biomarker and therapeutic potentials of FoxM1 in Glioma.