Aloe-emodin inhibits nasopharyngeal carcinoma by modulating telomerase activity involving the c-Myc/E2F1 axis.

Authors

Mengqin Li, Chunhong Li, Xin Zeng, Jiahua Hu, Han Su, Jiayi Huang, Min He, Jianhong Tang

Published in

Frontiers in pharmacology. Volume 17. Pages 1850685. Epub Jul 20, 2026.

Abstract

The telomerase catalytic subunit hTERT is a critical oncogenic driver in nasopharyngeal carcinoma (NPC). The specific role of aloe-emodin (AE) in regulating hTERT in NPC has not been systematically investigated. The regulatory network involving hTERT and its upstream transcription factors, c-Myc and E2F1, offers a promising therapeutic avenue.
Bioinformatics was used to analyze hTERT expression and its prognostic significance in head and neck squamous cell carcinoma and nasopharyngeal carcinoma. Molecular docking simulations were conducted to investigate the potential interaction between AE and hTERT. hTERT expression was assessed in normal nasal epithelial cells and NPC cell lines. Effects of AE on hTERT, c-Myc, and E2F1 were measured using qRT-PCR and Western blotting. Telomerase activity was evaluated through TRAP-qPCR and PAGE. hTERT was knocked down using siRNA. Cell proliferation, migration, and invasion were analyzed using CCK-8, EdU, colony formation, and Transwell assays. ROS levels were quantified using DCFH-DA staining. In vivo, a subcutaneous xenograft model was established to assess AE's anti-tumor efficacy alone and with shRNA-mediated hTERT knockdown. Organ toxicity was evaluated by H&E staining. Tumor tissues were analyzed by immunohistochemistry for hTERT, c-Myc, E2F1, Ki-67, and Cleaved Caspase-3.
Bioinformatics analysis revealed elevated hTERT expression in HNSC tissues and NPC cell lines Molecular docking predicted a potential interaction between AE and the catalytic pocket of hTERT. In vitro, AE treatment decreased c-Myc, increased E2F1, and reduced hTERT transcription. AE also reduced telomerase activity, increased ROS levels, and suppressed proliferation, migration, and invasion in NPC cells. In vivo, AE showed anti-tumor activity. Combined with hTERT knockdown, AE produced synergistic tumor suppression and enhanced modulation of the c-Myc/E2F1/hTERT axis and oxidative stress. Immunohistochemistry revealed suppressed proliferation and increased apoptosis in tumor tissues of the combination group. No significant organ toxicity was observed.
This study presents the first systematic validation of AE's anti-NPC effects. These include hTERT suppression, modulation of the c-Myc/E2F1 network, and induction of oxidative stress. These findings suggest a potential therapeutic target and strategy for NPC. The results support the clinical translation of AE.

PMID:
42548826
Bibliographic data and abstract were imported from PubMed on 04 Aug 2026.

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