Lysine lactylation in the regulation of tumor biology.

Kla emerges as a pivotal post-translational modification that influences tumor biology through transcriptional regulation and non-histone protein modulation, with a specific focus on metabolic proteins. An intricate connection between lysine lactylation (Kla) and the tumor microenvironment emerges from the role of this modification in regulating tumor survival and immune functions. Potential therapeutic strategies based on modulating Kla, particularly through histone deacetylase inhibitors, raise the prospect of combination therapies and highlight the importance of understanding lactylation kinetics in key metabolic enzymes. Research on Kla requires a more comprehensive identification of the enzymes involved and the development of innovative methodologies for precise detection and quantification in clinical applications. We introduce the concept of a 'dual engine' effect of Kla that showcases its simultaneous impact on epigenetic regulation and metabolic adaptation, training immune cells, and fostering an immunosuppressive niche. Lysine lactylation (Kla), a newly discovered post-translational modification (PTM) of lysine residues, is progressively revealing its crucial role in tumor biology. A growing body of evidence supports its capacity of transcriptional regulation through histone modification and modulation of non-histone protein function. It intricately participates in a myriad of events in the tumor microenvironment (TME) by orchestrating the transitions of immune states and augmenting tumor malignancy. Its preferential modification of metabolic proteins underscores its specific regulatory influence on metabolism. This review focuses on the effect and the probable mechanisms of Kla-mediated regulation of tumor metabolism, the upstream factors that determine Kla intensity, and its potential implications for the clinical diagnosis and treatment of tumors. [ABSTRACT FROM AUTHOR]