Abstract
As the end-product of glycolysis, lactate serves as a regulator of protein lactylation in addition to being an energy substrate, metabolite, and signaling molecule in cancer. The reprogramming of glucose metabolism and the Warburg effect in breast cancer results in extensive lactate production and accumulation, making it likely that lactylation in tumor tissue is also abnormal. This review summarizes evidence on lactylation derived from studies of lactate metabolism and disease, highlighting the role of lactate in the tumor microenvironment of breast cancer and detailing the levels of lactylation and cancer-promoting mechanisms across various tumors. The roles of lactate and lactylation, along with potential intervention mechanisms, are presented and discussed, offering valuable insights for future research on the role of lactylation in tumors.