E2F7 as a Dual Regulator of Tumor Suppression and Chemoresistance in Glioblastoma multiforme

Background Glioblastoma multiforme (GBM) is the most aggressive form of brain cancer, and chemoresistance poses a significant challenge to the survival and prognosis of GBM. Although numerous regulatory mechanisms contributing to chemoresistance have been identified, many questions remain unanswered. This study aims to identify the mechanism of temozolomide (TMZ) resistant in GBM. Methods Since a temozolomide (TMZ) resistance model in vivo has been published in our group, the present study has employed transcriptome sequencing and experiments to analyze the function of E2F7 in GBM during the TMZ treatment, and the ChIPBase and PROMO database was used to explore the upregulators of E2F7 in TMZ resistance tumors, further in vivo and in vitro experiments are required to confirm the results. Results The study revealed that E2F7 was significantly upregulated in TMZ resistant tumors, high expression of E2F7 inhibited GBM tumorigenesis and growth, and promoted chemoresistance by reducing drug uptake and facilitating efflux. Furthermore, we observed increased phosphorylation and activation of the p53 protein in TMZ-resistant tumors, which directly contributed to the transcriptional upregulation of E2F7. Conclusions E2F7 serves as a poor prognostic indicator for GBM, and potentially plays a crucial role in promotion of TMZ resistance, and the activation of the p53 protein in these TMZ resistance, which directly contributed to the transcriptional upregulation of E2F7.