ArticleOncology letters2016
Resistance to the c-Met inhibitor KRC-108 induces the epithelial transition of gastric cancer cells.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Harnessing Natural Products to Surmount Drug Resistance in Gastric Cancer: Mechanisms and Therapeutic Perspectives.International journal of biological sciences · 2025Review
- Synergistic Effects of the Combinational Use of Escitalopram Oxalate and 5-Fluorouracil on the Inhibition of Gastric Cancer SNU-1 Cells.International journal of molecular sciences · 2022Article
- Therapeutic Efficacy of ABN401, a Highly Potent and Selective MET Inhibitor, Based on Diagnostic Biomarker Test inCancers · 2020Article
- Comprehensive review of targeted therapy for colorectal cancer.Signal transduction and targeted therapy · 2020Review
- Mechanisms of Acquired Resistance to Savolitinib, a Selective MET Inhibitor inJCO precision oncology · 2020Article
- Corosolic acid reduces 5‑FU chemoresistance in human gastric cancer cells by activating AMPK.Molecular medicine reports · 2018Article
- Current advances of targeting HGF/c-Met pathway in gastric cancer.Annals of translational medicine · 2018Review
- Targeting c-MET in gastrointestinal tumours: rationale, opportunities and challenges.Nature reviews. Clinical oncology · 2017Review
- Long non-coding RNAs in anti-cancer drug resistance.Oncotarget · 2017Review
- Curcumin sensitizes human gastric cancer cells to 5-fluorouracil through inhibition of the NFκB survival-signaling pathway.OncoTargets and therapy · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Investigation of the mechanisms of resistance to targeted therapies is essential as resistance acquired during treatment may lead to relapse or refractoriness to the therapy. Our previous study identified the small molecule KRC-108 as a result of efforts to find an anticancer agent with c-Met-inhibitory activity. In the present study, the changes accompanying resistance to KRC-108 were investigated in the gastric cancer cell line MKN-45 and its KRC-108-resistant clones by western blot and immunofluorescence analyses. Increased expression of the c-Met protein was observed in KRC-108-resistant cells compared with that of the parental cells, and the phosphorylation of c-Met also increased in cell lines resistant to KRC-108. Resistance to the c-Met inhibitor was associated with cell morphological changes: MKN-45 parental cells, which had a round and poorly differentiated morphology, were altered to exhibit an epithelial cell-like phenotype in KRC-108-resistant clones. Consistent with the transition to an epithelial morphology, the expression of E-cadherin was increased in resistant cells. Using immunoprecipitation, an interaction between E-cadherin and the c-Met protein was observed in the KRC-108-resistant cells. Immunohistochemical analysis of human gastric carcinoma tissues revealed the co-expression of E-cadherin and c-Met. These results suggest that the epithelial transition in KRC-108-resistant cells is mediated by recruiting E-cadherin to c-Met protein. Thus, the present study identified a mechanism used by cancer cells to confer resistance to anticancer agents.
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