ArticleJournal of translational medicine2025
MCAM interacts with integrin β1 to promote EGFR-TKI resistance in lung adenocarcinoma through the JAK3 signalling pathway.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Melanoma cell adhesion molecule (MCAM) mediates microtentacle generation, homotypic clustering, and reattachment of non-adherent breast tumor cells.Breast cancer research : BCR · 2026Article
- PMADS: an integrated database of curated and proteomics-inferred associations between protein post-translational modifications and drug sensitivity.Nucleic acids research · 2026Article
- From EGFR PTM network to TKI resistance: spatial subtypes and targeting in lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2026Review
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14 authors.
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Abstract
backgroundEpidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have exhibited remarkable efficacy against EGFR-mutated lung cancer. However, the majority of patients receiving EGFR-TKIs face a grim prognosis due to acquired drug resistance. Melanoma cell adhesion molecule (MCAM), a highly glycosylated type I transmembrane protein belonging to the immunoglobulin superfamily, is upregulated in EGFR-TKI-resistant EGFR-mutant lung adenocarcinoma. The objective of this study was to investigate the role and mechanism of MCAM in mediating resistance to EGFR-TKIs.
methodsqRT-PCR, Western blot, and immunofluorescence techniques were employed to analyze the expression of MCAM in EGFR-TKI sensitive and resistant cells.CCK-8 assay and subcutaneous xenograft model in nude mice were utilized to investigate the correlation between MCAM expression level and resistance to EGFR-TKIs. Furthermore, receptor tyrosine kinase (RTK) phosphorylation antibody array, co-immunoprecipitation, immunofluorescence, and dual-luciferase assay were employed to elucidate its molecular mechanism.
resultsThe expression level of MCAM was significantly higher in EGFR-TKI resistant lung adenocarcinoma cells compared to EGFR-TKI sensitive lung adenocarcinoma cells. CCK-8 cytotoxicity assay demonstrated that overexpression of MCAM enhanced resistance to EGFR-TKIs in EGFR-mutant lung adenocarcinoma cells. Overexpression of MCAM promoted the growth of transplanted tumors in nude mice, while having a limited effect on the efficacy of EGFR-TKIs. Moreover, interaction between MCAM and integrin β1 activated the downstream JAK3 signaling pathway, thereby promoting resistance to EGFR-TKIs. The transcription factor STAT2 activates transcription of the target gene MCAM by binding to its promoter region.
conclusionsMCAM can enhance the resistance of EGFR-mutant lung adenocarcinoma cells to EGFR-TKIs, both in vitro and in vivo. Through its interaction with integrin β1, MCAM activates JAK3 protein, thereby stimulating cell proliferation and contributing to the development of acquired resistance in sensitive cell lines. The expression of MCAM is regulated by the transcription factor STAT2. This study presents a novel therapeutic strategy for patients with EGFR-TKI resistance.
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