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Background <p>Lung 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.</p> Methods <p>GMFB 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.</p> Results <p>GMFB 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. </p> Conclusions <p>GMFB promotes LUAD progression by activating the MAPK/ERK pathway, positioning it as a potential biomarker and therapeutic target for LUAD diagnosis and treatment.</p>

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GMFB promotes lung adenocarcinoma progression by activating the MAPK/ERK signaling pathway

  • 期刊论文

  • 发表日期：

    2026年4月11日

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  • Luyuan Ma,
  • Jiacheng Li,
  • Wenhao Yu,
  • Rongyang Li,
  • Libo Si

摘要

Background

Lung 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.

Methods

GMFB 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.

Results

GMFB 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.

Conclusions

GMFB promotes LUAD progression by activating the MAPK/ERK pathway, positioning it as a potential biomarker and therapeutic target for LUAD diagnosis and treatment.