EGFR/EGFRvIII partly regulates the tumourigenesis of glioblastoma through the SOX9-GLUT3 axis

EGFR/EGFR variant III (EGFRvIII) glioblastoma is seriously malignant, and the underlying mechanism remains unclear. In this study, EGFR and GLUT3 were found to be co-expressed in our collected tissues and associated with worse overall survival in glioblastoma via bioinformatics analysis. Functionally, in vitro and in vivo tests revealed that silencing GLUT3 substantially inhibited the viability of U87-EGFRvIII and LN229-EGFRvIII cells. Compared with wild-type U87 or LN229 cells, the expression level of SOX9 in U87-EGFRvIII or LN229-EGFRvIII cells (U87 and LN229 over-expressing EGFRvIII) was substantially increased. Chromatin immunoprecipitation and Dual-luciferase reporter assays revealed that SOX9 bound to the promoter of GLUT3 and promoted the expression of GLUT3. Collectively, our findings indicated that the EGFR/EGFRvIII-SOX9-GLUT3 axis mediated the tumourigenesis of glioblastoma and might be a potential target for glioblastoma therapy.

Automated summary

EGFR/EGFR variant III (EGFRvIII) glioblastoma with co-expression of EGFR and GLUT3 is associated with worse overall survival. Experimental evidence suggests that EGFRvIII and GLUT3 cooperate in promoting tumorigenesis, indicating a potential therapeutic target.