- Lactylation of tumour suppressor proteins alters their function and promotes immune tolerance, contributing to hepatocellular carcinoma progression.
- Molecular mechanisms of lactylation-driven immune escape in HCC remain incompletely understood and require further elucidation.
- Inhibiting lactylation represents a potential strategy to restore tumour suppressor function and enhance HCC immunotherapy efficacy.
Chin Med J (Engl). 2026 Aug 28. doi: 10.1097/CM9.0000000000004225. Online ahead of print.
ABSTRACT
Hepatocellular carcinoma (HCC) is the most common primary liver cancer and the third leading cause of cancer-related death worldwide. The etiology of liver cancer is complex and diverse; it is mainly caused by hepatitis virus infection, liver cirrhosis, and/or alcoholic hepatitis, among other contributing factors. However, the complex pathogenesis of HCC remains to be elucidated. Tumor suppressor proteins can inhibit the occurrence and development of tumors. Posttranslational modifications (PTMs) of proteins affect protein function, and lactylation is an important form of PTM. Recent studies have reported that after lactylation, tumor suppressor proteins regulate various biological processes, such as tumor immune tolerance. Therefore, lactylation of tumor suppressor proteins may promote the occurrence and development of HCC. Since the immune escape of HCC after lactylation of tumor suppressor proteins has rarely been reported, the exact molecular mechanism has not yet been clarified. In this article, we comprehensively analyzed the functional changes in tumor suppressor proteins after lactylation modification and reviewed the effects on immune escape in HCC and its regulatory mechanism, to identify targets for the development of lactylation inhibitors to enhance immunotherapy of HCC.
PMID:42665962 | DOI:10.1097/CM9.0000000000004225
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