ArticleMolecular and cellular biochemistry2026
GMFB promotes lung adenocarcinoma progression by activating the MAPK/ERK signaling pathway.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLung adenocarcinoma (LUAD) is a highly malignant tumor with a dismal prognosis worldwide. Glial maturation factor β (GMFB), initially identified as a regulator of glial cell development, has recently been implicated in tumor microenvironment-mediated carcinogenesis. This study aims to validate the role of GMFB in LUAD progression and explore its potential as a novel biomarker and therapeutic target.
methodsGMFB expression was evaluated in LUAD tissues and cell lines using bioinformatics analysis, immunohistochemistry (IHC), Western blotting (WB), and quantitative real-time PCR (qRT-PCR). In vitro functional assays (CCK-8, EdU, colony formation, transwell, wound healing) and a nude mouse subcutaneous tumor model were used to assess the effects of GMFB on cell proliferation and migration. RNA sequencing and bioinformatics were employed to identify downstream pathways, with rescue experiments confirming mechanistic insights.
resultsGMFB was significantly overexpressed in LUAD tissues and cell lines, and high GMFB expression was associated with poor patient survival. Functional studies showed that GMFB knockdown attenuated LUAD cell proliferation and migration, whereas GMFB overexpression promoted these phenotypes. In vivo experiments confirmed GMFB-driven tumor growth. Mechanistically, RNA sequencing and WB analysis revealed that GMFB activated the MAPK/ERK signaling pathway, and pharmacological inhibition of ERK reversed GMFB-mediated tumor progression.
conclusionsGMFB promotes LUAD progression by activating the MAPK/ERK pathway, positioning it as a potential biomarker and therapeutic target for LUAD diagnosis and treatment.
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