ERCC6L-mediated stabilization of HIF-1α enhances glycolysis and stemness properties of lung adenocarcinoma cells.

ABSTRACT: Molecular signatures are increasingly recognized as pivotal factors in therapy selection for lung adenocarcinomas (LUAD). A developing therapeutic approach focuses on targeting metabolic dependencies within cancer cells. ERCC6L, a vital protein involved in chromosome separation during cell mitosis, emerges as a compelling subject concerning its impact on LUAD tumorigenesis and progression. Our investigation uncovered elevated levels of ERCC6L in LUAD, significantly associated with unfavorable patient outcomes. Functional analyses elucidate ERCC6L's role in promoting LUAD cell proliferation, migration, and invasion by inducing glycolysis and stemness characteristics. Mechanistically, our data reveal ERCC6L's involvement in upregulating aerobic glycolysis through the induction of hypoxia-ind

SUBMITTER: Lu Z 

PROVIDER: S-EPMC12280123 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature