ArticleFrontiers in pharmacology2025
Aloe-emodin mediates the inhibitory effect of LncRNA D63785 on the PI3K/Akt/mTOR pathway in nasopharyngeal carcinoma.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Mechanism of miR-188-5p enhancing radioresistance in nasopharyngeal carcinoma by targeting PTEN to activate the PI3K/Akt signaling pathway.Translational cancer research · 2026Article
- Phytochemistry, Bioavailability, and Molecular Mechanisms Underlying Multitarget Anticancer Activity ofNutrients · 2026Review
- Aloe-emodin inhibits nasopharyngeal carcinoma by modulating telomerase activity involving the c-Myc/E2F1 axis.Frontiers in pharmacology · 2026Article
- Therapeutic effect of sustained release of aloe emodin via novel grafted polymer in electrospun nanofiber membranes on peritendinous adhesions.Frontiers in bioengineering and biotechnology · 2026Article
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9 authors.
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Abstract
Background: Long non-coding RNAs (lncRNAs) are dysregulated in nasopharyngeal carcinoma (NPC), yet their interplay with pharmacological agents like aloe-emodin (AE) remains unclear. This study explores AE's anti-NPC mechanisms via lncRNA D63785 and the PI3K/Akt/mTOR pathway. Methods: NPC cells (CNE1, C666-1) were treated with AE, followed by qRT-PCR and Western blotting to assess lncRNA D63785 and PI3K/Akt/mTOR pathway proteins. siRNA-mediated lncRNA D63785 knockdown combined with functional assays (CCK-8, EdU, colony/wound-healing) evaluated AE's effects on proliferation, migration, and pathway activity. Results: LncRNA D63785 was overexpressed in NPC cells (p < 0.01). AE suppressed lncRNA D63785 expression, concurrently reducing PI3K/Akt/mTOR phosphorylation (p < 0.05). siRNA knockdown partially reversed AE's inhibition of NPC cell viability, proliferation, and migration. Conclusion: AE exerts anti-NPC effects by targeting the lncRNA D63785-PI3K/Akt/mTOR axis, offering a novel therapeutic strategy. These findings bridge AE's pharmacological activity with lncRNA regulatory networks in NPC pathogenesis.
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