Research Progress in the Regulatory Mechanisms of Lactylation in Tumor Development and Therapy

长期以来，乳酸被认为是缺氧条件下通过糖酵解产生的代谢废物。然而，随着Warburg效应的发现，研究者认识到，即使在有氧条件下，肿瘤细胞依然能通过糖酵解途径产生乳酸。近年来的研究进一步揭示，乳酸不仅在肿瘤代谢重编程中发挥关键作用，还参与了一种新型的表观遗传修饰——乳酸化。乳酸化修饰对基因转录、蛋白质稳定性、代谢重编程、免疫逃逸及耐药性等肿瘤生物学特性产生深远影响。对乳酸化修饰机制的进一步探索，不仅加深了我们对肿瘤发生发展机制的理解，也为癌症治疗策略提供了新的思路。因此，本文总结了乳酸化在癌症研究中的最新进展，深入解析其在肿瘤生物学功能中的作用机制，并探讨其对癌症治疗的应用价值。Traditionally, lactate was considered as a metabolic waste product produced through glycolysis under hypoxic conditions. However, with the discovery of the Warburg effect, it has become evident that tumor cells can produce lactate via the glycolytic pathway even in the presence of oxygen. Recent studies have revealed that lactate not only plays a key role in tumor metabolic reprogramming, but also regulates a novel epigenetic modification known as lactylation. This modification has profound impact on tumor biological properties such as gene transcription, protein stability, metabolic reprogramming, immune escape and drug resistance. With further exploration of the mechanisms of lactylation modification, our understanding of tumorigenesis and progression has been significantly expanded, which provides new ideas for cancer therapeutic strategies. Therefore, this paper summarizes the recent advances of lactylation research in cancer, elucidates its functional mechanisms in tumor biology, and explores its potential implications for therapeutic strategies.