Hepatocellular carcinoma (HCC) is a malignant tumor characterized by profound metabolic reprogramming and a pronounced Warburg effect, resulting in excessive lactate accumulation in the tumor microenvironment (TME). Traditionally regarded as a metabolic byproduct, lactate has recently been recognized as a substrate for lactylation, offering new insights into tumorigenesis and cancer progression. The present review systematically summarized the molecular basis of lactylation and delineated its regulatory network in HCC. It focused on how lactylation contributes to the malignant phenotype of HCC cells and reshapes the TME, highlighting its roles in tumor progression and metabolic‑immune interactions. Based on current evidence, lactylation‑related features show potential translational value in the diagnosis, treatment and prognosis of HCC. A deeper understanding of lactylation mechanisms may provide novel insights and strategies for precision therapy in HCC.
Chen et al. (Thu,) studied this question.