Secretion of acetylated amino acids by drug-induced cancer cells: perspectives on metabolic-epigenetic alterations

The emerging understanding of the super-complex and heterogeneous nature of tumor is well supported by metabolic reprogramming, leading survival advantages. Metabolic reprogramming contributes to tumor responsiveness and resistance to various antitumor drugs. Among the numerous adaptations made by cancer cells in response to drug-induced perturbations, key metabolic alterations involving amino acids and acetylated derivatives of amino acids have received special attention. Considering these implications discussed, targeting cancer-associated metabolic pathways, particularly those involving acetylated amino acids, emerges as an important avenue in the pursuit of combinatorial anticancer strategies. As a result, the introduction of mimetic acetylated amino acids represents a promising new class of inhibitors that could be used alongside traditional chemotherapy agents. Cancer cells are known to show complexity and resistance to treatment, including chemotherapies and radiation therapies. The ability of cancer cells to overcome effects of anticancer drugs are related to metabolic changes. One of key forms of metabolic changes is in the form of acetylation of amino acids that promote survival of cancer cells in various settings in cancer patients. Therefore, a better understanding of metabolic changes in the context of acetylation of amino acids could help better manage the treatment of cancer patients. Among various mechanisms adopted by cancer cells, acetylation of amino acids is considered a key to metabolic reprogramming in drug resistance. Exploring mimetics of acetylated amino acids as an anticancer drug specific to protein targets and membrane transporters is proposed.