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Updated: Jan 23, 2026

Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis

Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis

Published on: August 9, 2013

ウイルス-宿主レドックス軸：EBNA1-FOSL2-ALDH3A1はEBV陽性癌における標的化可能な脆弱性を定義する

Qian Liu¹, Binliang Liu², Zhenbao Liu³

¹Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, 410013, PR China; Key Laboratory of Carcinogenesis and Invasion, Chinese Ministry of Education, Cancer Research Institute, Xiangya School of Basic Medical Science, Central South University, Changsha, Hunan, 410078, PR China.

|January 21, 2026

Abstract:

Epstein-Barr virus (EBV)-associated carcinomas exhibit reprogrammed redox metabolism, yet the underlying regulatory network and potential metabolic vulnerabilities remain incompletely defined. Here we identify a viral-host transcriptional axis in which EBV EBNA1 induces the transcription factor FOSL2 to repress ALDH3A1. Restoration of ALDH3A1 in EBV-positive models disrupts NAD(P)H/NAD(P)⁺ homeostasis, inducing reductive stress. This reductive milieu upregulates GSNOR and TrxR1, potentiating the denitrosylation of GSK3β, leading to its stabilization and suppression of the Wnt/β-catenin pathway. We establish that S-nitrosylation at GSK3β Cys199 controls its stability, providing a mechanistic bridge from redox regulation to Wnt inhibition. Critically, ALDH3A1 elevation selectively curbs EBV-positive tumor growth, exploiting an infection-specific vulnerability in redox signaling. Thus, our findings integrate EBV-driven redox remodeling with Wnt/β-catenin signaling activation and propose ALDH3A1 induction as a promising therapeutic strategy for EBV-associated carcinomas.

キーワード:

ALDH3A1 EBNA1 EBV癌レドックス Wnt/β-カテニンシグナル伝達

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