ArticleInternational journal of molecular sciences2014
Cetuximab-induced MET activation acts as a novel resistance mechanism in colon cancer cells.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 36 citations in OpenAlex.
- A randomized, placebo-controlled, phase 1/2 study of tivantinib (ARQ 197) in combination with irinotecan and cetuximab in patients with metastatic colorectal cancer with wild-type KRAS who have received first-line systemic therapy.International journal of cancer · 2016Trial
- SFTA2 reduced colorectal cancer ferroptosis promoting metastasis through regulating EMT transition by degradation of Nrf2.Food & nutrition research · 2026Article
- circ-EGFR is a predictor of response to Cetuximab and a potential target in colorectal cancer.EMBO molecular medicine · 2025Article
- Evolving roles of MET as a therapeutic target in NSCLC and beyond.Nature reviews. Clinical oncology · 2025Review
- Exploring Predictive and Prognostic Biomarkers in Colorectal Cancer: A Comprehensive Review.Cancers · 2024Review
- c-Src inhibitor PP2 inhibits head and neck cancer progression through regulation of the epithelial-mesenchymal transition.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- M2PP: a novel computational model for predicting drug-targeted pathogenic proteins.BMC bioinformatics · 2022Article
- Emerging actionable targets to treat therapy-resistant colorectal cancers.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies.Journal of experimental & clinical cancer research : CR · 2021Review
- Analysis of transient membrane protein interactions by single-molecule diffusional mobility shift assay.Experimental & molecular medicine · 2021Article
- Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications.Cancers · 2020Review
- RANKL/RANK promotes the migration of gastric cancer cells by interacting with EGFR.Clinical and translational medicine · 2020Article
- An Fc-Optimized CD133 Antibody for Induction of Natural Killer Cell Reactivity against Colorectal Cancer.Cancers · 2019Article
- Article
- Caveolin‑1 enhances RANKL‑induced gastric cancer cell migration.Oncology reports · 2018Article
- c-Cbl Expression Correlates with Human Colorectal Cancer Survival and Its Wnt/β-Catenin Suppressor Function Is Regulated by Tyr371 Phosphorylation.The American journal of pathology · 2018Observational
- CXCL9/10/11, a regulator of PD-L1 expression in gastric cancer.BMC cancer · 2018Article
- ZEB1 inhibition sensitizes cells to the ATR inhibitor VE-821 by abrogating epithelial-mesenchymal transition and enhancing DNA damage.Cell cycle (Georgetown, Tex.) · 2018Article
- Protein biomarkers predictive for response to anti-EGFR treatment in RAS wild-type metastatic colorectal carcinoma.British journal of cancer · 2017Article
- A novel function of hepatocyte growth factor in the activation of checkpoint kinase 1 phosphorylation in colon cancer cells.Molecular and cellular biochemistry · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant MET expression and hepatocyte growth factor (HGF) signaling are implicated in promoting resistance to targeted agents; however, the induced MET activation by epidermal growth factor receptor (EGFR) inhibitors mediating resistance to targeted therapy remains elusive. In this study, we identified that cetuximab-induced MET activation contributed to cetuximab resistance in Caco-2 colon cancer cells. MET inhibition or knockdown sensitized Caco-2 cells to cetuximab-mediated growth inhibition. Additionally, SRC activation promoted cetuximab resistance by interacting with MET. Pretreatment with SRC inhibitors abolished cetuximab-mediated MET activation and rendered Caco-2 cells sensitive to cetuximab. Notably, cetuximab induced MET/SRC/EGFR complex formation. MET inhibitor or SRC inhibitor suppressed phosphorylation of MET and SRC in the complex, and MET inhibitor singly led to disruption of complex formation. These results implicate alternative targeting of MET or SRC as rational strategies for reversing cetuximab resistance in colon cancer.
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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.