Autophagy-dependent secretion of ENO1 mediates chemoresistance of glioblastoma and tumor microenvironment remodeling.

ABSTRACT: Acquired therapeutic resistance in glioblastoma multiforme (GBM) constitutes a major determinant of its refractory and tumor recurrence. Both tumor-intrinsic epigenetic regulation and tumor microenvironment (TME) remodeling are now understood to play pivotal roles in this resistance; however, the synergistic mechanisms and key molecular mediators underlying this interplay remain poorly defined. In this study, we demonstrated that temozolomide (TMZ) could activate the autophagy-dependent secretory pathway to promote extracellular secretion of Alpha-enolase (ENO1). Extracellular soluble ENO1 robustly enhanced GBM cell proliferation, migration, and invasion in vitro. Clinically, serum ENO1 levels were markedly elevated in GBM patients and strongly correlated with TMZ therapeutic response, sug

SUBMITTER: Xie Q 

PROVIDER: S-EPMC12827997 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature