ORIGINAL RESEARCH article

Front. Pharmacol.

Sec. Pharmacology of Anti-Cancer Drugs

Volume 16 - 2025 | doi: 10.3389/fphar.2025.1573408

This article is part of the Research TopicHead and Neck Squamous Cell Carcinoma: Navigating the Dawn of Personalized MedicineView all 9 articles

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

Provisionally accepted
Min HeMin He1Lei XieLei Xie2,3Jiayi HuangJiayi Huang1Han SuHan Su4Jiahua HuJiahua Hu1,5Liuping XieLiuping Xie2,3Mengqin LiMengqin Li2,3Xin ZengXin Zeng2,3Jianhong TangJianhong Tang1,5,6*
  • 1The Second Affiliated Hospital of Guilin Medical University, Guilin, China
  • 2School of Pharmacy, Guilin Medical University, Guilin, Guangxi Zhuang Region, China
  • 3Guangxi Key Laboratory of Diabetic Systems Medicine, Guilin Medical University, Guilin, Guangxi Zhuang Region, China
  • 4Department of Neurology, Affiliated Hospital of Guilin Medical University, Guilin, China
  • 5Central Laboratory, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, Guilin, China
  • 6School of General Medical, Guilin Medical University, Guilin, China

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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.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. In vivo validation used nude mouse xenografts.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. In vivo, AE attenuated tumor growth (p<0.05), correlating with lncRNA D63785 downregulation and PI3K/Akt/mTOR dephosphorylation.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.

Keywords: AE1, NPC2, LncRNA D637853, PI3K/Akt/mTOR signaling pathway4, Proliferation and migration5

Received: 09 Feb 2025; Accepted: 23 Jun 2025.

Copyright: © 2025 He, Xie, Huang, Su, Hu, Xie, Li, Zeng and Tang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Jianhong Tang, The Second Affiliated Hospital of Guilin Medical University, Guilin, China

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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