ArticleCurrent research in toxicology2025
The JPX/miR-495-3p/BRD4 axis mediates quercetin-induced toxicity via the X-inactivation center in NSCLC.
Article in Current research in toxicology, 2025. 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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Abstract
Background: Emerging evidence underscores the pivotal role of long non-coding RNAs (lncRNAs) as master regulators of oncogenic pathways, positioning them as compelling therapeutic targets in precision oncology. While the natural flavonoid quercetin has demonstrated potent anti-neoplastic activity against non-small cell lung cancer (NSCLC), its influence on lncRNA-mediated oncogenic pathways remains unknown. This study is designed to elucidate whether quercetin exerts its anti-NSCLC effects via modulation of lncRNA just proximal to XIST (JPX) and its downstream signaling axis. Methods: NSCLC cell lines were treated with quercetin, and functional assays (CCK-8, BrdU incorporation, scratch assay, and Transwell migration) were conducted to assess proliferation and metastatic potential. Gain- and loss-of-function experiments, combined with qPCR and western blotting, were performed to validate the JPX-modulated regulatory network. Results: Quercetin significantly suppressed NSCLC proliferation and migration by downregulating oncogenic JPX, which in turn upregulated tumor-suppressive miR-495-3p, leading to bromodomain-containing protein 4 (BRD4) suppression. JPX silencing mimicked quercetin's effects, while rescue experiments confirmed the JPX/miR-495-3p/BRD4 axis as critical for quercetin's activity. Conclusion: Our findings identify quercetin as a natural compound targeting the JPX-miR-495-3p-BRD4 cascade, providing both mechanistic insights and a translational rationale for quercetin-based NSCLC therapy. These findings highlight the therapeutic potential of quercetin in NSCLC and support further exploration of lncRNA-targeted strategies.
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