ArticleBMC cancer2016
Novel c-Met inhibitor suppresses the growth of c-Met-addicted gastric cancer cells.
Article in BMC cancer, 2016. 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, 41 citations in OpenAlex.
- Characterization of acquired capecitabine resistance in MKN-45 gastric cancer cells reveals preserved apoptotic sensitivity.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- Advancements in antibody-drug conjugates as cancer therapeutics.Journal of the National Cancer Center · 2025Review
- Comparative analysis of whole-genome sequencing of tumor and cfDNA in a neuroblastoma patient: a case report.Frontiers in oncology · 2025Article
- Research progress on the development of hepatocyte growth factor/c-Met signaling pathway in gastric cancer: A review.World journal of gastrointestinal oncology · 2024Review
- Ferroptosis regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.World journal of gastrointestinal oncology · 2024Article
- Characterization of MET Alterations in 37 Gastroesophageal Cancer Cell Lines for MET-Targeted Therapy.International journal of molecular sciences · 2024Article
- Patient-derived exosomes facilitate therapeutic targeting of oncogenic MET in advanced gastric cancer.Science advances · 2023Article
- Therapeutic Strategies for Ovarian Cancer in Point of HGF/c-MET Targeting.Medicina (Kaunas, Lithuania) · 2022Review
- Inhibitory effect of polyphenols (phenolic acids, lignans, and stilbenes) on cancer by regulating signal transduction pathways: a review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Opportunities and challenges of targeting c-Met in the treatment of digestive tumors.Frontiers in oncology · 2022Review
- Dual-function chimeric antigen receptor T cells targeting c-Met and PD-1 exhibit potent anti-tumor efficacy in solid tumors.Investigational new drugs · 2021Article
- Blockage of ETS homologous factor inhibits the proliferation and invasion of gastric cancer cells through the c-Met pathway.World journal of gastroenterology · 2020Article
- Inhibition of c-MET increases the antitumour activity of PARP inhibitors in gastric cancer models.Journal of cellular and molecular medicine · 2020Article
- Therapeutic Efficacy of ABN401, a Highly Potent and Selective MET Inhibitor, Based on Diagnostic Biomarker Test inCancers · 2020Article
- Model-based analysis of response and resistance factors of cetuximab treatment in gastric cancer cell lines.PLoS computational biology · 2020Article
- Review
- MET as resistance factor for afatinib therapy and motility driver in gastric cancer cells.PloS one · 2019Article
- Amplification of Wild-typeClinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Extracellular Matrix Influencing HGF/c-MET Signaling Pathway: Impact on Cancer Progression.International journal of molecular sciences · 2018Review
- HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundc-Met signaling has been implicated in oncogenesis especially in cells with c-met gene amplification. Since 20 % of gastric cancer patients show high level of c-Met expression, c-Met has been identified as a good candidate for targeted therapy in gastric cancer. Herein, we report our newly synthesized c-Met inhibitor by showing its efficacy both in vitro and in vivo.
methodsCompounds with both triazolopyrazine and pyridoxazine scaffolds were synthesized and tested using HTRF c-Met kinase assay. We performed cytotoxic assay, cellular phosphorylation assay, and cell cycle assay to investigate the cellular inhibitory mechanism of our compounds. We also conducted mouse xenograft assay to see efficacy in vivo.
resultsKRC-00509 and KRC-00715 were selected as excellent c-Met inhibitors through biochemical assay, and exhibited to be exclusively selective to c-Met by kinase panel assay. Cytotoxic assays using 18 gastric cancer cell lines showed our c-Met inhibitors suppressed specifically the growth of c-Met overexpressed cell lines, not that of c-Met low expressed cell lines, by inducing G1/S arrest. In c-met amplified cell lines, c-Met inhibitors reduced the downstream signals including Akt and Erk as well as c-Met activity. In vivo Hs746T xenograft assay showed KRC-00715 reduced the tumor size significantly.
conclusionsOur in vitro and in vivo data suggest KRC-00715 is a potent and highly selective c-Met inhibitor which may have therapeutic potential in gastric tumor with c-Met overexpression.
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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.