ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013
Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- The role of c-Met and VEGFR2 in glioblastoma resistance to bevacizumab.Scientific reports · 2021Trial
- Targeting MET and mTOR Synergistically Overcomes Adaptive Resistance in Glioblastoma.International journal of molecular sciences · 2026Article
- Distinct cMET inhibitors uncover pharmacological heterogeneity in SHH medulloblastoma cell lines.Discover oncology · 2026Article
- BNIP3-mTOR Signaling Mediates Resistance to MET Inhibition in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- Tyrosine Kinase Inhibitors for Glioblastoma Multiforme: Challenges and Opportunities for Drug Delivery.Pharmaceutics · 2022Review
- Targeting Angiogenic Factors for the Treatment of Medulloblastoma.Current treatment options in oncology · 2022Review
- HGF/MET Signaling in Malignant Brain Tumors.International journal of molecular sciences · 2020Review
- ShRNA-based POLD2 expression knockdown sensitizes glioblastoma to DNA-Damaging therapeutics.Cancer letters · 2020Article
- SPINT2 is hypermethylated in both IDH1 mutated and wild-type glioblastomas, and exerts tumor suppression via reduction of c-Met activation.Journal of neuro-oncology · 2019Article
- Discovery and Therapeutic Exploitation of Mechanisms of Resistance to MET Inhibitors in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Phase 1 trial, pharmacokinetics, and pharmacodynamics of dasatinib combined with crizotinib in children with recurrent or progressive high-grade and diffuse intrinsic pontine glioma.Pediatric blood & cancer · 2018Article
- Cancer stem cells from peritumoral tissue of glioblastoma multiforme: the possible missing link between tumor development and progression.Oncotarget · 2018Article
- The multiple paths towards MET receptor addiction in cancer.Oncogene · 2018Review
- Review
- Novel MET/TIE2/VEGFR2 inhibitor altiratinib inhibits tumor growth and invasiveness in bevacizumab-resistant glioblastoma mouse models.Neuro-oncology · 2016Article
- The hepatocyte growth factor receptor as a potential therapeutic target for dedifferentiated liposarcoma.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Article
- Exogenous HGF Bypasses the Effects of ErbB Inhibition on Tumor Cell Viability in Medulloblastoma Cell Lines.PloS one · 2015Article
- Constitutive and ligand-induced EGFR signalling triggers distinct and mutually exclusive downstream signalling networks.Nature communications · 2014Article
- microRNA-148a is a prognostic oncomiR that targets MIG6 and BIM to regulate EGFR and apoptosis in glioblastoma.Cancer research · 2014Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
purposeThe receptor tyrosine kinase (RTK) c-MET and its ligand hepatocyte growth factor (HGF) are deregulated and promote malignancy in cancer and brain tumors. Consequently, clinically applicable c-MET inhibitors have been developed. The purpose of this study was to investigate the not-well-known molecular determinants that predict responsiveness to c-MET inhibitors and to explore new strategies for improving inhibitor efficacy in brain tumors. EXPERIMENTAL
designWe investigated the molecular factors and pathway activation signatures that determine sensitivity to c-MET inhibitors in a panel of glioblastoma and medulloblastoma cells, glioblastoma stem cells, and established cell line-derived xenografts using functional assays, reverse protein microarrays, and in vivo tumor volume measurements, but validation with animal survival analyses remains to be done. We also explored new approaches for improving the efficacy of the inhibitors in vitro and in vivo.
resultsWe found that HGF coexpression is a key predictor of response to c-MET inhibition among the examined factors and identified an ERK/JAK/p53 pathway activation signature that differentiates c-MET inhibition in responsive and nonresponsive cells. Surprisingly, we also found that short pretreatment of cells and tumors with exogenous HGF moderately but statistically significantly enhanced the antitumor effects of c-MET inhibition. We observed a similar ligand-induced sensitization effect to an EGF receptor small-molecule kinase inhibitor.
conclusionsThese findings allow the identification of a subset of patients that will be responsive to c-MET inhibition and propose ligand pretreatment as a potential new strategy for improving the anticancer efficacy of RTK inhibitors.
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