ArticleInternational journal of oncology2016
MEK inhibitors against MET-amplified non-small cell lung cancer.
Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Systematic analysis of the transcriptional landscape of melanoma reveals drug-target expression plasticity.Briefings in functional genomics · 2025Article
- Emerging AXL Inhibitors in Oncology: Chemical and Biological Advances in Targeted Cancer Therapy.Anti-cancer agents in medicinal chemistry · 2025Review
- Combining mechanistic quantitative systems pharmacology modeling and patient-derived organoid testing in MET-aberrant non-small cell lung cancer for high-throughput combination efficacy analysis and personalized treatment design.Frontiers in pharmacology · 2025Article
- Mesoporous silica nanoparticles: a versatile carrier platform in lung cancer management.Nanomedicine (London, England) · 2024Review
- Targeting MEK in non-small cell lung cancer.Current problems in cancer · 2024Review
- PAI-1 mediates acquired resistance to MET-targeted therapy in non-small cell lung cancer.PloS one · 2024Article
- βIII-tubulin suppression enhances the activity of Amuvatinib to inhibit cell proliferation in c-Met positive non-small cell lung cancer cells.Cancer medicine · 2023Article
- Molecular Biology and Therapeutic Perspectives for K-Ras Mutant Non-Small Cell Lung Cancers.Cancers · 2022Review
- TargetingFrontiers in oncology · 2022Review
- Activation of Receptor Tyrosine Kinases Mediates Acquired Resistance to MEK Inhibition in Malignant Peripheral Nerve Sheath Tumors.Cancer research · 2021Article
- Case Report: High-Level MET Amplification as a Resistance Mechanism of ROS1-Tyrosine Kinase Inhibitors in ROS1-Rearranged Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Article
- [Chinese Expert Consensus on Next Generation Sequencing Diagnosis for Non-small Cell Lung Cancer (2020 Edition)].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020Article
- Acquired BRAF Rearrangements Induce Secondary Resistance to EGFR therapy in EGFR-Mutated Lung Cancers.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2019Article
- miR‑146a‑5p targets TCSF and influences cell growth and apoptosis to repress NSCLC progression.Oncology reports · 2019Article
- IL-17A promotes cell migration and invasion of glioblastoma cells via activation of PI3K/AKT signalling pathway.Journal of cellular and molecular medicine · 2019Article
- The expression of HOXA13 in lung adenocarcinoma and its clinical significance: A study based on The Cancer Genome Atlas, Oncomine and reverse transcription-quantitative polymerase chain reaction.Oncology letters · 2018Article
- Novel 3D Liquid Cell Culture Method for Anchorage-independent Cell Growth, Cell Imaging and Automated Drug Screening.Scientific reports · 2018Article
- Clinical implication of UCA1 in non-small cell lung cancer and its effect on caspase-3/7 activation and apoptosis induction in vitro.International journal of clinical and experimental pathology · 2018Article
- Driver genes in non-small cell lung cancer: Characteristics, detection methods, and targeted therapies.Oncotarget · 2017Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several receptor tyrosine kinases (RTKs) including EGFR, ALK, and MET have been identified as therapeutic targets in non-small cell lung cancer (NSCLC). Among the downstream pathways of RTKs, the MAPK pathway is particularly important for cancer cell proliferation, differentiation, and survival. In this study, the effects of MEK inhibitors (trametinib and PD0325901) in several NSCLC cell lines with driver gene alterations, especially RTK genes, were tested in vitro using an MTT assay, and a wide range of sensitivities was found. In particular, all the EGFR-mutated cell lines were resistant to MEK inhibitors, whereas all the MET-amplified cell lines were sensitive. A bioinformatics technique and western blot analyses showed that the PI3K/AKT pathway is more activated in EGFR-mutated NSCLC than in MET-amplified NSCLC, and a PI3K inhibitor enhanced the sensitivity to trametinib in the EGFR-mutated cell lines, suggesting that this pathway is associated with resistance to MEK inhibitors. Although the HCC827 cell line (EGFR mutation) was resistant to MEK inhibitors, the HCC827CNXR cell line, whose driver gene shifts from EGFR to MET, exhibited enhanced sensitivity to MEK inhibitors, indicating the biological importance of the MAPK pathway for MET-amplified NCSLC. Furthermore, a synergistic effect of crizotinib (a MET inhibitor) and trametinib was observed in MET-amplified NCLC cell lines. Our findings indicate that the MAPK pathway is biologically important for MET-amplified NSCLC and strongly encourage the development of combination therapy with a MET inhibitor and a MEK inhibitor against MET-amplified NSCLC.
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