Aloe-emodin mediates the inhibitory effect of LncRNA D63785 on the PI3K/Akt/mTOR pathway in nasopharyngeal carcinoma

Aloe-emodin mediates the inhibitory effect of LncRNA D63785 on the PI3K/Akt/mTOR pathway in nasopharyngeal carcinoma

BackgroundLong 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.MethodsNPC cells (CNE1, C66...

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Main Authors: Min He, Lei Xie, Jiayi Huang, Han Su, Jiahua Hu, Liuping Xie, Mengqin Li, Xin Zeng, Jianhong Tang
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-07-01
Series:Frontiers in Pharmacology
Subjects:
AE
NPC
LncRNA D63785
PI3K/Akt/mTOR signaling pathway
proliferation and migration
Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2025.1573408/full
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Summary:BackgroundLong 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.MethodsNPC 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. In vivo validation used nude mouse xenografts.ResultsLncRNA 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. In vivo, AE attenuated tumor growth (p < 0.05), correlating with lncRNA D63785 downregulation and PI3K/Akt/mTOR dephosphorylation.ConclusionAE 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.
ISSN:1663-9812

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