ArticleCancer research2008
Met and c-Src cooperate to compensate for loss of epidermal growth factor receptor kinase activity in breast cancer cells.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 126 citations in OpenAlex.
- Review
- Article
- Overcoming resistance to targeted therapy using MET inhibitors in solid cancers: evidence from preclinical and clinical studies.Medical oncology (Northwood, London, England) · 2021Review
- When the MET receptor kicks in to resist targeted therapies.Oncogene · 2021Review
- Chemotherapeutic drugs: Cell death- and resistance-related signaling pathways. Are they really as smart as the tumor cells?Translational oncology · 2021Review
- Exposure to chewing tobacco promotes primary oral squamous cell carcinoma and regional lymph node metastasis by alterations of SDF1α/CXCR4 axis.International journal of experimental pathology · 2021Article
- Targeting c-Met in triple negative breast cancer: preclinical studies using the c-Met inhibitor, Cpd A.Investigational new drugs · 2020Article
- Analysis of the Effect of Increased α2,3-Sialylation on RTK Activation in MKN45 Gastric Cancer Spheroids Treated with Crizotinib.International journal of molecular sciences · 2020Article
- Thiosemicarbazones suppress expression of the c-Met oncogene by mechanisms involving lysosomal degradation and intracellular shedding.The Journal of biological chemistry · 2020Article
- Elevated FAM83A expression predicts poorer clincal outcome in lung adenocarcinoma.Cancer biomarkers : section A of Disease markers · 2019Article
- The Importance of the Right Framework: Mitogen-Activated Protein Kinase Pathway and the Scaffolding Protein PTPIP51.International journal of molecular sciences · 2018Review
- Effectiveness of EGFR/HER2-targeted drugs is influenced by the downstream interaction shifts of PTPIP51 in HER2-amplified breast cancer cells.Oncogenesis · 2018Article
- Receptor tyrosine kinases (RTKs) in breast cancer: signaling, therapeutic implications and challenges.Molecular cancer · 2018Review
- Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities.Molecular cancer · 2018Review
- Lignans Isolated From Flower Buds ofFrontiers in pharmacology · 2018Article
- Analysis of progress and challenges for various patterns of c-MET-targeted molecular imaging: a systematic review.EJNMMI research · 2017Review
- Multiplexed Exchange-PAINT imaging reveals ligand-dependent EGFR and Met interactions in the plasma membrane.Scientific reports · 2017Article
- Dual inhibition of MET and SRC kinase activity as a combined targeting strategy for colon cancer.Experimental and therapeutic medicine · 2017Article
- Ran GTPase promotes cancer progression via Met recepto-rmediated downstream signaling.Oncotarget · 2016Article
- Impact of the putative cancer stem cell markers and growth factor receptor expression on the sensitivity of ovarian cancer cells to treatment with various forms of small molecule tyrosine kinase inhibitors and cytotoxic drugs.International journal of oncology · 2016Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Breast cancers are not responsive to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI), although 30% of breast cancers overexpress EGFR. The mechanism of intrinsic resistance to EGFR TKIs in breast cancer is the focus of current studies. Here, we observed that EGFR remains tyrosine phosphorylated in breast cancer cells that proliferate in the presence of EGFR TKIs. In one such cell line, SUM229, inhibiting c-Src kinase activity with either a dominant-negative c-Src or a c-Src TKI decreased EGFR phosphorylation on Tyr(845), Tyr(992), and Tyr(1086) in the presence of EGFR TKIs. Conversely, overexpressing wild-type (wt) c-Src in the EGFR TKI-sensitive breast cancer cell line SUM149 increased EGFR kinase-independent EGFR tyrosine phosphorylation. In addition, in the presence of EGFR TKIs, inhibiting c-Src kinase activity decreased cell growth in SUM229 cells, and overexpressing wt-c-Src increased cell growth in SUM149 cells. We identified the receptor tyrosine kinase Met to be responsible for activating c-Src in SUM229 cells. Inhibiting Met kinase activity with a small molecule inhibitor decreased c-Src phosphorylation and kinase activation. In addition, inhibiting Met kinase activity in SUM229 cells decreased EGFR tyrosine phosphorylation and growth in the presence of EGFR TKIs. Stimulating Met kinase activity in SUM149 cells with hepatocyte growth factor increased EGFR tyrosine phosphorylation and cell growth in the presence of EGFR TKIs. These data suggest a Met/c-Src-mediated signaling pathway as a mediator of EGFR tyrosine phosphorylation and cell growth in the presence of EGFR TKIs.
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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.