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Article

MiR-23c Regulates the Resistance to Gefitinib in EGFR Mutant Non-Small-Cell Lung Cancer Cells.

Cells - 6 Jun 2026

Ignoto Brigitta, Parisi Ilaria Assunta, Roma Cristin, Camerlingo Rosa, Dotolo Serena, Tufano Salvatore, Maiello Monica Rosaria, Normanno Nicola, Morabito Alessandro, De Luca Antonella, Frezzetti Daniela

Abstract excerpt

Mechanisms of primary and acquired resistance are responsible for treatment failure with the Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors (EGFR-TKIs) in the majority of patients with advanced Non-Small-Cell Lung Cancer (NSCLC) carrying EGFR-activating mutations. MicroRNAs (miRNAs) are important modulators of EGFR signaling in lung cancer. Recent studies suggested the role of miR-23c as a tumor...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 42346070
DOI: 10.3390/cells15121043
PMCID: PMC13296432

Genes

EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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MiR-23c Regulates the Resistance to Gefitinib in EGFR Mutant Non-Small-Cell Lung Cancer Cells.PMID 42346070Read ↗

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.Semantic proximity Read ↗

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miR-19a contributes to gefitinib resistance and epithelial mesenchymal transition in non-small cell lung cancer cells by targeting c-MetSemantic proximity Read ↗

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MiR-130a Overcomes Gefitinib Resistance by Targeting Met in Non-Small Cell Lung Cancer Cell LinesSemantic proximity Read ↗

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Activation of IL-6R/JAK1/STAT3 signaling induces de novo resistance to irreversible EGFR inhibitors in non-small cell lung cancer with T790M resistance mutation.Semantic proximity Read ↗

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