ArticleAmerican journal of translational research2025
Mesenchymal stem cells promote erlotinib resistance in non-small cell lung cancer through the HGF-AKT/ERK1/2-OPN pathway.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Mesenchymal stem cell-induced metabolic reprogramming of EGFR-wild-type tumor cells drives therapeutic resistance in EGFR-mutant non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Harnessing transcriptomics for discovery of natural products to overcome acquired cancer resistance.Archives of pharmacal research · 2026Review
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6 authors.
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Abstract
objectivesTo investigate the mechanisms by which mesenchymal stem cells (MSCs) contribute to erlotinib resistance in non-small cell lung cancer (NSCLC).
methodsHCC827 NSCLC cells were treated with MSC-conditioned medium (MSC-CM). Cell viability and apoptosis were evaluated using MTT assays and flow cytometry, respectively. Protein and mRNA expression levels were assessed by western blotting and quantitative real-time PCR. For
resultsMSC-CM significantly increased cell viability and reduced apoptosis in HCC827 cells following erlotinib treatment, indicating enhanced drug resistance. Mechanistically, MSC-secreted hepatocyte growth factor (HGF) activated AKT and ERK1/2 phosphorylation, thereby bypassing EGFR inhibition by erlotinib. Neutralization of HGF restored erlotinib sensitivity in MSC-CM-treated HCC827 cells. Furthermore, osteopontin (OPN) was transcriptionally upregulated and acted as a resistance enhancer. Inhibition of OPN attenuated MSC-CM-mediated resistance.
conclusionsThis study identifies a novel MSC-mediated resistance mechanism in which MSC-derived HGF activates compensatory AKT/ERK1/2 signaling, circumventing EGFR blockade by erlotinib. Concurrent upregulation of OPN in NSCLC cells forms a synergistic survival axis under erlotinib pressure. These findings suggest that targeting MSC-derived HGF and tumor-derived OPN may offer promising strategies to overcome erlotinib resistance in NSCLC.
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