ArticleJournal of molecular signaling2010
EGFR/Met association regulates EGFR TKI resistance in breast cancer.
Article in Journal of molecular signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The trial behind it
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Who cites it
58 citing papers in PubMed, 96 citations in OpenAlex.
- Article
- Review
- Cross-Talk between NOK and EGFR: Juxtamembrane and Kinase domain interactions enhancing STAT3/5 signaling in breast cancer tumorigenesis.Translational oncology · 2025Article
- A Conjugate of an EGFR-Binding Peptide and Doxorubicin Shows Selective Toxicity to Triple-Negative Breast Cancer Cells.ACS medicinal chemistry letters · 2025Article
- The impact of 9-azaglycophymine and phenylguanidine derivatives on the proliferation of various breast cancer cell lines in vitro and in vivo.Scientific reports · 2024Article
- Hsp90 inhibition leads to an increase in surface expression of multiple immunological receptors in cancer cells.Frontiers in molecular biosciences · 2024Article
- Combinations of EGFR and MET inhibitors reduce proliferation and invasiveness of mucosal melanoma cells.Journal of cellular and molecular medicine · 2023Article
- Candida albicans stimulates formation of a multi-receptor complex that mediates epithelial cell invasion during oropharyngeal infection.PLoS pathogens · 2023Article
- Article
- ELF4 is a critical component of a miRNA-transcription factor network and is a bridge regulator of glioblastoma receptor signaling and lipid dynamics.Neuro-oncology · 2023Article
- Article
- Foretinib Is Effective against Triple-Negative Breast Cancer Cells MDA-MB-231 In Vitro and In Vivo by Down-Regulating p-MET/HGF Signaling.International journal of molecular sciences · 2023Article
- Design, Synthesis and In Vitro Investigation of Cabozantinib-Based PROTACs to Target c-Met Kinase.Pharmaceutics · 2022Article
- Conjugation of Cetuximab - Puromycin and Its Target-Specific Effect on Triple Negative Breast Cancer Cell Lines.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Anticancer Effects and Molecular Action of 7-α-Hydroxyfrullanolide in G2/M-Phase Arrest and Apoptosis in Triple Negative Breast Cancer Cells.Molecules (Basel, Switzerland) · 2022Article
- MET overexpression contributes to STAT4-PD-L1 signaling activation associated with tumor-associated, macrophages-mediated immunosuppression in primary glioblastomas.Journal for immunotherapy of cancer · 2021Article
- A Need for More Molecular Profiling in Brain Metastases.Frontiers in oncology · 2021Review
- MET amplification results in heterogeneous responses to osimertinib in EGFR-mutant lung cancer treated with erlotinib.Cancer science · 2020Article
- Expression level of EGFR and MET receptors regulates invasiveness of melanoma cells.Journal of cellular and molecular medicine · 2019Article
- EGFL9 promotes breast cancer metastasis by inducing cMET activation and metabolic reprogramming.Nature communications · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancers show a lack of response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), despite 30% of tumors expressing EGFR. The mechanism of this resistance is unknown; however, we have recently shown that Met kinase activity compensates for loss of EGFR kinase activity in cell culture models. Met has been implicated in the pathogenesis of breast tumors and therefore may cooperate with EGFR for tumor growth. Here we have found that EGFR phosphorylation and cell proliferation is in part regulated by Met expression. In addition, we found that Met constitutive phosphorylation occurred independent of the Met ligand hepatocyte growth factor (HGF). Ligand-independent Met phosphorylation is mediated by Met amplification, mutation, or overexpression and by Met interaction with other cell surface molecules. In SUM229 breast cancer cells, we found that Met was not amplified or mutated, however it was overexpressed. Met overexpression did not directly correlate with ligand-independent Met phosphorylation as the SUM229 cell line was the only Met expressing breast cancer line with constitutive Met phosphorylation. Interestingly, Met expression did correlate with EGFR expression and we identified an EGFR/Met complex via co-immunoprecipitation. However, we only observed Met constitutive phosphorylation when c-Src also was part of this complex. Ligand-independent phosphorylation of Met was decreased by down regulating EGFR expression or by inhibiting c-Src kinase activity. Lastly, inhibiting EGFR and Met kinase activities resulted in a synergistic decrease in cell proliferation, supporting the idea that EGFR and Met functionally, as well as physically interact in breast cancer cells to regulate response to EGFR inhibitors.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.