ACSS2-mediated acetyl-CoA accumulation promotes mitophagy and tumor growth via increased H3K27ac in HBV-related HCC
These findings not only illustrate the interplay between metabolic reprogramming, epigenetic modification, and tumorigenesis in the context of HBV infection, but also highlight ACSS2 as a novel metabolic vulnerability in HBV-related HCC. Therefore, targeting ACSS2 could be a novel strategy against HBV-associated HCC.
Authors
- Ailong Huang (ORCID: https://orcid.org/0000-0003-0148-7423)
- Xin Tang (ORCID: https://orcid.org/0000-0002-9237-7109)
- Xiao Dong (ORCID: https://orcid.org/0000-0002-4687-8324)
- Yihan Yan (ORCID: https://orcid.org/0009-0008-1078-1492)
- Shan Li (ORCID: https://orcid.org/0000-0002-8134-263X)
- Rong Zhang (ORCID: https://orcid.org/0000-0003-1188-0640)
- Xinrui Liu (ORCID: https://orcid.org/0000-0003-2348-5891)
- Jie Hu (ORCID: https://orcid.org/0000-0002-3368-0183)
- Kai Wang (ORCID: https://orcid.org/0000-0003-0567-3004)
- Ni Tang (ORCID: https://orcid.org/0000-0003-0456-4789)
- Huijun Liang (ORCID: https://orcid.org/0000-0001-7344-1489)
- Yuan Hu
- Junji Tao
Institutions
- People's Hospital of Bishan District (CN)
- Chongqing Emergency Medical Center (CN)
- Chongqing Medical University (CN)
Publication Details
- Journal
- Clinical and Molecular Hepatology
- Published
- 2025-12-19
- DOI
- https://doi.org/10.3350/cmh.2025.0754
- Primary Topic
- Cancer, Hypoxia, and Metabolism
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Chinese Academy of Sciences
- Tsinghua University
- Chongqing Medical University
- National Key Research and Development Program of China