Wang Cuicui, Ma Xiaoxin
Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang City, Liaoning Province, China.
Key Laboratory of Gynecological Oncology of Liaoning Province, Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
Clin Transl Med. 2025 Jan;15(1):e70145. doi: 10.1002/ctm2.70145.
As a hallmark of cancer, metabolic reprogramming adjusts macromolecular synthesis, energy metabolism and redox homeostasis processes to adapt to and promote the complex biological processes of abnormal growth and proliferation. The complexity of metabolic reprogramming lies in its precise regulation by multiple levels and factors, including the interplay of multiple signalling pathways, precise regulation of transcription factors and dynamic adjustments in metabolic enzyme activity. In this complex regulatory network, acetylation and deacetylation, which are important post-translational modifications, regulate key molecules and processes related to metabolic reprogramming by affecting protein function and stability. Dysregulation of acetylation and deacetylation may alter cancer cell metabolic patterns by affecting signalling pathways, transcription factors and metabolic enzyme activity related to metabolic reprogramming, increasing the susceptibility to rapid proliferation and survival. In this review, we focus on discussing how acetylation and deacetylation regulate cancer metabolism, thereby highlighting the central role of these post-translational modifications in metabolic reprogramming, and hoping to provide strong support for the development of novel cancer treatment strategies. KEY POINTS: Protein acetylation and deacetylation are key regulators of metabolic reprogramming in tumour cells. These modifications influence signalling pathways critical for tumour metabolism. They modulate the activity of transcription factors that drive gene expression changes. Metabolic enzymes are also affected, altering cellular metabolism to support tumour growth.
作为癌症的一个标志，代谢重编程可调节大分子合成、能量代谢和氧化还原稳态过程，以适应并促进异常生长和增殖等复杂的生物学过程。代谢重编程的复杂性在于其受到多个层面和多种因素的精确调控，包括多种信号通路的相互作用、转录因子的精确调控以及代谢酶活性的动态调节。在这个复杂的调控网络中，乙酰化和去乙酰化作为重要的翻译后修饰，通过影响蛋白质功能和稳定性来调节与代谢重编程相关的关键分子和过程。乙酰化和去乙酰化的失调可能通过影响与代谢重编程相关的信号通路、转录因子和代谢酶活性来改变癌细胞的代谢模式，增加癌细胞快速增殖和存活的易感性。在本综述中，我们重点讨论乙酰化和去乙酰化如何调节癌症代谢，从而突出这些翻译后修饰在代谢重编程中的核心作用，并希望为新型癌症治疗策略的开发提供有力支持。要点：蛋白质乙酰化和去乙酰化是肿瘤细胞代谢重编程的关键调节因子。这些修饰影响对肿瘤代谢至关重要的信号通路。它们调节驱动基因表达变化的转录因子的活性。代谢酶也受到影响，改变细胞代谢以支持肿瘤生长。
