Sirtuin 3-mediated delactylation of malic enzyme 2 disrupts redox balance and inhibits colorectal cancer growth
This study reveals that ME2 K352 lactylation is a critical regulatory mechanism that modulates enzymatic activity, mitochondrial function, and tumor progression. SIRT3-mediated delactylation of ME2 K352 disrupts redox homeostasis and inhibits tumor growth. These findings highlight the potential of targeting ME2 lactylation as a therapeutic strategy in cancer treatment.
Authors
- Hang‐Dong Jia
- Surui Yao (ORCID: https://orcid.org/0000-0002-1585-8101)
- Chang-Wen Ge
- Peng Teng (ORCID: https://orcid.org/0000-0002-7412-9646)
- Zhaohui Huang (ORCID: https://orcid.org/0000-0002-0117-9976)
- Chaoqun Li (ORCID: https://orcid.org/0000-0002-3087-2884)
- Qingwen Wang (ORCID: https://orcid.org/0000-0001-5988-9922)
Institutions
- Jiangnan University (CN)
- Wuxi Fourth People's Hospital (CN)
Publication Details
- Journal
- Cellular Oncology
- Published
- 2025-04-07
- DOI
- https://doi.org/10.1007/s13402-025-01058-5
- Citations
- 6
- Primary Topic
- Cancer, Hypoxia, and Metabolism
- Type
- article
- Field-Weighted Citation Impact
- 5.62
Funders
- National Natural Science Foundation of China
- Government of Jiangsu Province
- Basic Research Program of Jiangsu Province