ArticleMolecular cancer therapeutics2014
Off-target effects of c-MET inhibitors on thyroid cancer cells.
Article in Molecular cancer therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
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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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- A systematic review of emerging RNA markers in thyroid fine needle aspiration cytology samples: advancements and challenges.Endocrine · 2025Pooled it
- Discovery of 2H-Pyrrolo[3,4‑ACS medicinal chemistry letters · 2026Article
- Distinct cMET inhibitors uncover pharmacological heterogeneity in SHH medulloblastoma cell lines.Discover oncology · 2026Article
- New insights into the tumor immune microenvironment and immunotherapy of thyroid cancer.Frontiers in immunology · 2026Review
- Overexpressed MET drives aggressive thyroid cancer phenotypes and serves as a precision therapeutic target.Scientific reports · 2025Article
- Cell Component and Function of Tumor Microenvironment in Thyroid Cancer.International journal of molecular sciences · 2022Review
- Recent Research Progress of Chiral Small Molecular Antitumor-Targeted Drugs Approved by the FDA From 2011 to 2019.Frontiers in oncology · 2021Review
- Novel Molecular Challenges in Targeting Anaplastic Lymphoma Kinase in ALK-Expressing Human Cancers.Cancers · 2017Review
- The role of signal transducer and activator of transcription 3 in Rift Valley fever virus infection.Virology · 2016Article
- Molecular profiles of cancer stem-like cell populations in aggressive thyroid cancers.Endocrine · 2016Article
- Integrating Murine and Clinical Trials with Cabozantinib to Understand Roles of MET and VEGFR2 as Targets for Growth Inhibition of Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Crizotinib-induced antitumour activity in human alveolar rhabdomyosarcoma cells is not solely dependent on ALK and MET inhibition.Journal of experimental & clinical cancer research : CR · 2015Article
- KRAS and HRAS mutations confer resistance to MET targeting in preclinical models of MET-expressing tumor cells.Molecular oncology · 2015Article
- Impact of MET targeting on tumor-associated angiogenesis and growth of MET mutations-driven models of liver cancer.Genes & cancer · 2015Article
- Comparison of microarray expression profiles between follicular variant of papillary thyroid carcinomas and follicular adenomas of the thyroid.BMC genomics · 2015Article
- Tivantinib in MET-high hepatocellular carcinoma patients and the ongoing Phase III clinical trial.Hepatic oncology · 2014Review
- Radioactive iodine-refractory differentiated thyroid cancer: an uncommon but challenging situation.Archives of endocrinology and metabolismReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
Aberrantly activated c-MET signaling occurs in several cancers, promoting the development of c-MET inhibitors. In this study, we found that eight of eight thyroid cancer cell lines (including six anaplastic thyroid cell lines) have prominent expression of c-MET protein. Fifty percent of the thyroid cancer cell lines (four of eight) were growth inhibited by two small molecule c-MET inhibitors (tivantinib and crizotinib) associated with apoptosis and G(2)-M cell-cycle arrest. However, crizotinib did not inhibit 50% proliferation of thyroid cancer cells (SW1736 and TL3) at a concentration at which the drug completely inhibited ligand-stimulated c-MET phosphorylation. However, tivantinib was less potent than crizotinib at inhibiting c-MET phosphorylation, but was more potent than crizotinib at decreasing cell growth. Suppressing c-MET protein expression and phosphorylation using siRNA targeting c-MET did not induce cell-cycle arrest and apoptosis. Taken together, tivantinib and crizotinib have off-target(s) activity, contributing to their antitumor activity. In vivo study showed that crizotinib markedly inhibited the growth of thyroid cancer cells (SW1736) in immunodeficient mice. In summary, c-MET inhibitors (tivantinib and crizotinib) suppress the growth of aggressive thyroid cancer cells, and this potential therapeutic benefit results from their non-MET-targeting effects.
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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.