Protein lactylation: molecular mechanisms underlying lactate-driven tumorigenesis and cancer progression.

IF 5.7 4区 医学 Q2 ONCOLOGY
Cancer Biology & Therapy Pub Date : 2025-12-31 Epub Date: 2025-12-18 DOI:10.1080/15384047.2025.2603081
Qianyun Xie, Lijuan Weng, Yuqing Hu, Qingsong Tao, Ruishuang Ma
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引用次数: 0

Abstract

Lactylation, a recently identified post-translational modification, has reshaped our understanding of lactate from a metabolic byproduct to a central regulator of tumor biology. Accumulating evidence reveals that lactate-driven lactylation orchestrates metabolic reprogramming, epigenetic remodeling, immune evasion, metastasis, and therapeutic resistance, thereby fueling malignant progression. Beyond histones, diverse non-histone substrates further expand its regulatory network across cancer signaling pathways. We highlight the crosstalk between lactylation and other modifications, its role in tumor heterogeneity, and the therapeutic opportunities arising from targeting this pathway. These insights establish lactylation as both a hallmark and a potential vulnerability of cancer, opening new avenues for precision oncology.

蛋白质乳酸化:乳酸驱动的肿瘤发生和癌症进展的分子机制。
乳酸化,最近发现的翻译后修饰,重塑了我们对乳酸从代谢副产物到肿瘤生物学中心调节器的理解。越来越多的证据表明,乳酸驱动的乳酸化协调代谢重编程、表观遗传重塑、免疫逃避、转移和治疗抵抗,从而促进恶性进展。除了组蛋白之外,多种非组蛋白底物进一步扩展了其在癌症信号通路中的调节网络。我们强调了乳酸化和其他修饰之间的串扰,它在肿瘤异质性中的作用,以及针对这一途径产生的治疗机会。这些见解确立了乳酸化既是癌症的标志,也是癌症的潜在脆弱性,为精确肿瘤学开辟了新的途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cancer Biology & Therapy
Cancer Biology & Therapy 医学-肿瘤学
CiteScore
7.00
自引率
0.00%
发文量
60
审稿时长
2.3 months
期刊介绍: Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
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