ArticleScientific reports2017
miR-19a contributes to gefitinib resistance and epithelial mesenchymal transition in non-small cell lung cancer cells by targeting c-Met.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- MiR-23c Regulates the Resistance to Gefitinib in EGFR Mutant Non-Small-Cell Lung Cancer Cells.Cells · 2026Article
- A Robust NSCLC Biomarker- miR-7-5p: ItsMicroRNA (Shariqah, United Arab Emirates) · 2025Article
- MicroRNA-130a-3p regulates osimertinib resistance by targeting runt-related transcription factor 3 in lung adenocarcinoma.Scientific reports · 2024Article
- Non-Coding RNAs as Key Regulators in Lung Cancer.International journal of molecular sciences · 2023Review
- MicroRNAs and Drug Resistance in Non-Small Cell Lung Cancer: Where Are We Now and Where Are We Going.Cancers · 2022Review
- MiRNAs in Lung Cancer: Diagnostic, Prognostic, and Therapeutic Potential.Diagnostics (Basel, Switzerland) · 2022Review
- <em>miR-19a</em> targeting <em>CLCA4</em> to regulate the proliferation, migration, and invasion of colorectal cancer cells.European journal of histochemistry : EJH · 2022Article
- MicroRNAs as the critical regulators of tyrosine kinase inhibitors resistance in lung tumor cells.Cell communication and signaling : CCS · 2022Review
- miRNAs in anti-cancer drug resistance of non-small cell lung cancer: Recent advances and future potential.Frontiers in pharmacology · 2022Review
- Application Value of Serum Multi-Antibody Combined Detection in Differential Diagnosis and Typing of Lung Cancer.Journal of oncology · 2022Article
- Role of miRNA-19a in Cancer Diagnosis and Poor Prognosis.International journal of molecular sciences · 2021Review
- Overexpression of CTEN is associated with gefitinib resistance in non-small cell lung cancer.Oncology letters · 2021Article
- Downregulation of miR-19a inhibits the proliferation and promotes the apoptosis of osteosarcoma cells by regulating the JAK2/STAT3 pathway.Oncology letters · 2020Article
- Dynamical network analysis reveals key microRNAs in progressive stages of lung cancer.PLoS computational biology · 2020Article
- Non-Coding RNAs in Lung Tumor Initiation and Progression.International journal of molecular sciences · 2020Review
- Article
- Crosstalk Mechanisms Between HGF/c-Met Axis and ncRNAs in Malignancy.Frontiers in cell and developmental biology · 2020Review
- MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.Frontiers in cell and developmental biology · 2020Review
- miR-762 activation confers acquired resistance to gefitinib in non-small cell lung cancer.BMC cancer · 2019Article
- Berberine induces apoptosis in non-small-cell lung cancer cells by upregulating miR-19a targeting tissue factor.Cancer management and research · 2019Article
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8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, is used as a first-line treatment for advanced non-small cell lung cancer (NSCLC). However, most NSCLC patients inevitably develop gefitinib resistance, and the mechanisms underlying this resistance are not fully understood. In this study, we show that miR-19a is significantly down-regulated in gefitinib-resistant NSCLC cell lines compared with gefitinib-sensitive cell lines. In addition, the down-regulation of miR-19a suppressed the expression of epithelial markers but induced the expression levels of mesenchymal markers. A mechanistic analysis revealed that miR-19a regulated c-Met expression by directly targeting the c-Met 3'UTR. Overexpression of miR-19a decreased c-Met expression and re-sensitized gefitinib-resistant NSCLC cells in vitro and in vivo. Consistent with the in vitro findings, the miR-19a serum level was significantly decreased in NSCLC patients with acquired gefitinib resistance compared with the level observed prior to the acquisition of resistance in each patient, indicating that miR-19a expression may be a valuable biomarker for the prediction of acquired gefitinib resistance in a clinical setting. Our data demonstrate that the miR-19a/c-Met pathway plays a critical role in acquired resistance to gefitinib and that the manipulation of miR-19a might provide a therapeutic strategy for overcoming acquired gefitinib resistance.
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