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<p>Non-small cell lung cancer (NSCLC) is a highly prevalent and aggressive malignancy, where early diagnosis and therapeutic intervention are pivotal for enhancing patient prognosis. Nonetheless, the lack of reliable biomarkers remains a substantial hurdle in clinical practice. In this study, we identified dysregulated microRNAs (miRNAs) in NSCLC, revealing a significant downregulation of miR-3202 and an upregulation of miR-3182. We demonstrate that both miR-3202 and miR-3182 play critical roles in modulating NSCLC cell proliferation and motility. Notably, we identify DTL as a direct target of miR-3202, with sustained expression of DTL reversing the effects of miR-3202 on cell growth and migration. Mechanistically, we show that miR-3202 regulates the ubiquitination and proteasomal degradation of p21 through DTL. These findings provide novel insights into the miRNA landscape in NSCLC and underscore the functional significance of the miR-3202–DTL–p21 axis. Our results position miR-3202 as a potential biomarker for NSCLC, thereby offering a foundation for the development of targeted diagnostic and therapeutic strategies.</p>

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MiR-3202–DTL signaling axis impedes NSCLC malignancy via regulating the ubiquitination-proteasome degradation of p21

  • 期刊论文

  • 发表日期：

    2025年3月4日

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  • Hongjuan Guo,
  • Qianbin Tang,
  • Yujie Zhao,
  • Jianghao Cheng,
  • JunJie Wang,
  • Dan Liu,
  • Ruyu Yan,
  • Dongjin Lv,
  • Bingxiao Lu,
  • Mingsong Wu,
  • Hongtao Yu,
  • Hao Leng,
  • Bo Liu,
  • Minxia Liu,
  • Kecheng Zhou

摘要

Non-small cell lung cancer (NSCLC) is a highly prevalent and aggressive malignancy, where early diagnosis and therapeutic intervention are pivotal for enhancing patient prognosis. Nonetheless, the lack of reliable biomarkers remains a substantial hurdle in clinical practice. In this study, we identified dysregulated microRNAs (miRNAs) in NSCLC, revealing a significant downregulation of miR-3202 and an upregulation of miR-3182. We demonstrate that both miR-3202 and miR-3182 play critical roles in modulating NSCLC cell proliferation and motility. Notably, we identify DTL as a direct target of miR-3202, with sustained expression of DTL reversing the effects of miR-3202 on cell growth and migration. Mechanistically, we show that miR-3202 regulates the ubiquitination and proteasomal degradation of p21 through DTL. These findings provide novel insights into the miRNA landscape in NSCLC and underscore the functional significance of the miR-3202–DTL–p21 axis. Our results position miR-3202 as a potential biomarker for NSCLC, thereby offering a foundation for the development of targeted diagnostic and therapeutic strategies.