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<p>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.</p>

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

  • 期刊论文

  • 发表日期：

    2026年1月13日

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

摘要

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.