ArticleMolecular and cellular biochemistry2025
MiR-3202-DTL signaling axis impedes NSCLC malignancy via regulating the ubiquitination-proteasome degradation of p21.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
15 authors.
Funding
Abstract
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.
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Registered trials
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