Intracellular and exosomal miR-101-3p regulated by METTL14 confers Gefitinib sensitivity in NSCLC.

Qinglong Kong, Ling Wu, Jun Li, Haoyu Wang, Chundong Gu

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Article in Medical oncology (Northwood, London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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5 authors.

Qinglong KongDalian Medical University, Dalian, 116044, Liaoning, People's Republic of China.

Ling WuDepartment of Thoracic Surgery, Dalian Municipal Central Hospital, Dalian, 116033, Liaoning, People's Republic of China.

Jun LiDepartment of Thoracic Surgery, Dalian Municipal Central Hospital, Dalian, 116033, Liaoning, People's Republic of China.

Haoyu WangDepartment of Thoracic Surgery, Dalian Municipal Central Hospital, Dalian, 116033, Liaoning, People's Republic of China.

Chundong GuDalian Medical University, Dalian, 116044, Liaoning, People's Republic of China. guchundong@dmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gefitinib Resistance (GR) is a frequent occurrence for non-small cell lung cancer (NSCLC). Here, we aim to explore a novel miR-101-3p shuttled by NSCLC cells in the growth and metastasis of NSCLC cells. Real-time PCR was performed to assess the level of miR-101-3p in cells and exosomes derived from the NSCLC cells. Effect of miR-101-3p on cell proliferation, metastasis and gefitinib sensitivity was then detected. Instinctively, METTL14 expression level was detected, which was positively related to that of miR-101-3p. Function of METTL14 on cell proliferation and metastasis was also investigated. High level of exosomal and intracellular miR-101-3p is correlated with better gefitinib response. miR-101-3p inhibited NSCLC cell proliferation and migration. In terms of mechanism, METTL14 endow NSCLC cells with gefitinib sensitivity via intracellular and exosomal miR-101-3p, leading to modulating of GSK-3β/Akt pathway. Collectively, this study indicated that restored METTL14/miR-101-3p confers gefitinib sensitivity in GR NSCLC by targeting GSK-3β/Akt pathway, indicating METTL14/miR-101-3p may act as a potential biomarker and therapeutic target for gefitinib response in NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungGefitinibLung NeoplasmsMethyltransferasesMicroRNAsAntineoplastic AgentsCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmExosomesGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansProto-Oncogene Proteins c-aktAntineoplastic AgentsGefitinibGlycogen Synthase Kinase 3 betaMethyltransferasesMETTL14 protein, humanMicroRNAsMIRN101 microRNA, humanProto-Oncogene Proteins c-aktExosomal miR-101-3pGefitinibMETTL14NSCLC

Identifiers

PMID41528401

DOI10.1007/s12032-026-03242-5

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