Yes-associated protein 1 in cancer: bridging mechanical transduction and epigenetic regulation.

IF 4.6 4区医学 Q2 ONCOLOGY

Cancer Biology & Therapy Pub Date : 2025-12-31 Epub Date: 2025-09-21 DOI:10.1080/15384047.2025.2562726

Tingting Liu, Shuo Yu, Lu Zhang, Wenwen Ji, Guangdong Wang, Na Wang, Mengcong Li, Tinghua Hu, Zhihong Shi

引用次数: 0

Abstract

Yes-associated protein 1 (YAP1) and its paralog TAZ serve as central mechanotransductive transcription coactivators that integrate mechanical cues from the extracellular matrix, such as stiffness and fluid shear stress, with epigenetic modifications to drive oncogenic processes. They regulate diverse biological functions, including proliferation, metastasis, immune evasion, autophagy, ferroptosis, and metabolism. This review highlights how YAP1/TAZ signaling is modulated by mechanosensitive pathways (Integrin/FAK, Rho GTPases) and epigenetic mechanisms (m6A methylation, DNA methylation), contributing to therapy resistance and disease progression. Targeting the mechano-epigenetic axis of YAP1/TAZ offers promising therapeutic strategies for cancer treatment.

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癌症中的yes相关蛋白1：桥接机械转导和表观遗传调控。

yes相关蛋白1 （YAP1）及其平行TAZ作为中心机械转导转录共激活因子，将来自细胞外基质的机械信号（如刚度和流体剪切应力）与表观遗传修饰整合在一起，以驱动致癌过程。它们调节多种生物功能，包括增殖、转移、免疫逃避、自噬、铁下垂和代谢。这篇综述强调了YAP1/TAZ信号是如何通过机械敏感途径（Integrin/FAK, Rho GTPases）和表观遗传机制（m6A甲基化，DNA甲基化）调节的，有助于治疗耐药和疾病进展。靶向YAP1/TAZ的机械-表观遗传轴为癌症治疗提供了有希望的治疗策略。

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 医学-肿瘤学

CiteScore

7.00

自引率

0.00%

发文量

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.