ArticleCell biology and toxicology2025
U2AF65 mediated circPVT1 promotes NSCLC cell proliferation and inhibits ferroptosis through the miR-338-3p/GPX4 axis.
Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- TRERNA1-mediated acetylation represses ferroptosis of non-small cell lung cancer cells via the KAT6A/H3K23ac/TRIM24-PIK3CA pathway.Human cell · 2026Article
- Targeting ferroptosis in lung cancer: pharmacological regulation, nanomedicine-based delivery, and AI-enabled translational strategies.American journal of cancer research · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
backgroundDysregulation of circRNA expression is associated with increased metastasis and an adverse prognosis in non-small cell lung cancer (NSCLC). Herein, this study assessed the role and regulatory mechanism of circPVT1 in NSCLC development.
methodsCircPVT1 expression was determined using qPCR. Functional assays, including cell proliferation, colony formation, and ferroptosis-related measurements (ROS, MDA, SOD, GSH and Fe
resultsCircPVT1 was significantly elevated in NSCLC samples, correlating with worse clinical outcomes. Its knockdown resulted in diminished cell proliferation and increased ferroptosis. Mechanically, circPVT1 sponges miR-338-3p, facilitating GPX4 expression, which enhanced cell proliferation. U2AF65 bound to and stabilized circPVT1, promoting cell proliferation. In animal models, U2AF65 knockdown suppressed tumor progression by regulating the circPVT1/miR-338-3p/GPX4 signaling pathway.
conclusionsU2AF65 stabilizes circPVT1 to promote NSCLC advancement through miR-338-3p suppression and GPX4 upregulation. Thus, circPVT1 and U2AF65 may be potential therapeutic targets in NSCLC.
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