ArticleCancer biomarkers : section A of Disease markers2020
MiR-200c-3p suppression is associated with development of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in EGFR mutant non-small cell lung cancer via a mediating epithelial-to-mesenchymal transition (EMT) process.
Article in Cancer biomarkers : section A of Disease markers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Advances in miR‑200c regulation of apoptosis, pyroptosis and autophagy in disease (Review).Molecular medicine reports · 2026Review
- Astragaloside IV Co-Loaded Osimertinib Liposomes Alleviate EGFR-TKI Resistance in Non-Small Cell Lung Cancer.International journal of nanomedicine · 2026Article
- MicroRNA-200c Promotes Epithelial-Mesenchymal Transition of Lens Epithelial Cells by Activating the Yes-Associated Protein Signaling Pathway.Journal of ophthalmology · 2026Article
- The role of miRNAs in the development of brain metastases originating from lung adenocarcinoma.Frontiers in genetics · 2026Article
- Review
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- Epithelial-mesenchymal transition (EMT) and its role in acquired epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) chemoresistance in non-small cell lung cancer (NSCLC).Cancer pathogenesis and therapy · 2025Review
- MicroRNAs as Sensitizers of Tyrosine Kinase Inhibitor Resistance in Cancer: Small Molecule Partnerships.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Comprehensive microRNA expression analysis of pediatric gonadal germ cell tumors: unveiling novel biomarkers and signatures.Molecular oncology · 2024Article
- miR-204 suppresses cancer stemness and enhances osimertinib sensitivity in non-small cell lung cancer by targeting CD44.Molecular therapy. Nucleic acids · 2024Article
- Non-Coding RNAs as Key Regulators in Lung Cancer.International journal of molecular sciences · 2023Review
- Loss of Key EMT-Regulating miRNAs Highlight the Role of ZEB1 in EGFR Tyrosine Kinase Inhibitor-Resistant NSCLC.International journal of molecular sciences · 2023Article
- MicroRNAs Present in Malignant Pleural Fluid Increase the Migration of Normal Mesothelial Cells In Vitro and May Help Discriminate between Benign and Malignant Effusions.International journal of molecular sciences · 2023Article
- Exosome-derived circKIF20B suppresses gefitinib resistance and cell proliferation in non-small cell lung cancer.Cancer cell international · 2023Article
- The Profiling of Apoptosis-Associated MicroRNA Expressions of the Lung Adenocarcinoma.Thoracic research and practice · 2023Article
- Progress in the studies on the molecular mechanisms associated with multidrug resistance in cancers.Acta pharmaceutica Sinica. B · 2023Review
- MicroRNA-200c-3p Negatively Regulates ATP2A2 and Promotes the Progression of Papillary Thyroid Carcinoma.Biochemical genetics · 2022Article
- MiR-200c-3p and miR-485-5p overexpression elevates cisplatin sensitivity and suppresses the malignant phenotypes of non-small cell lung cancer cells through targeting RRM2.Thoracic cancer · 2022Article
- Functions of non-coding RNAs in regulating cancer drug targets.Acta biochimica et biophysica Sinica · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEGFR-mutant lung cancer inevitably develops resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs).
objectiveTo investigate the clinical relevance of microRNAs (miRNAs) in TKI therapy response and resistance.
methodsWe performed a miRNA PCR array analysis and used The Cancer Genome Atlas (TCGA) database to identify potential miRNAs related to EGFR TKIs resistance. We then correlated miRNA expression in 70 surgical and 50 malignant pleural effusion specimens with patient outcomes in those with non-small cell lung carcinoma. Molecular manipulation was performed in EGFR mutant lung cancer cells to assess the effect of miR-200c-3p on cell migratory ability and EGFR-TKI sensitivity.
resultsWe identified miR-200c-3p and miR-203a-3p as potential EGFR TKI resistance regulators via their modulation of epithelial-to-mesenchymal transition (EMT). MiR-200c-3p and miR-203a-3p were down-regulated in EGFR TKI-resistant cell lines. Progression-free survival (PFS) with EGFR-TKI treatment of patients with high miR-200c-3p expression, but not miR-203a-3p, in the specimens was significantly longer than that of patients with low expression. MiR-200c-3p overexpression inhibited the EMT process in EGFR TKI resistance cell lines and promoted cell death. MiR-200c-3p silencing in EGFR TKI sensitive cell lines increased drug resistance.
conclusionMiR-200c-3p plays a role in sensitivity to EGFR TKIs via modulating EMT process.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.