Hypoxia-induced PRMT6 expression promotes temozolomide chemoresistance in glioblastoma via G3BP1.

ABSTRACT:

Background

Glioblastoma multiforme (GBM), the most aggressive primary brain tumor, is associated with extremely poor patient prognosis. Temozolomide (TMZ) resistance remains a major cause of treatment failure. Protein arginine methyltransferase 6 (PRMT6) plays critical roles in tumorigenesis, but its function and regulatory mechanisms in GBM TMZ resistance have not been elucidated. While the hypoxic microenvironment is a hallmark feature of GBM, its epigenetic regulatory mechanisms in drug resistance remain unclear.

Methods

We analyzed PRMT6 expression and prognostic value in GBM using public databases (TCGA, CGGA). TMZ resistance was assessed through in vitro assays (CCK-8, flow cytometry, colony formation) and in vivo xenograft models. Molecular mechanisms of the HIF-1α/PR

SUBMITTER: Chen S 

PROVIDER: S-EPMC12903591 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature