基质刚度驱动的癌症进展和靶向治疗策略

Rui Liang, Guanbin Song
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摘要

基质刚度增加是实体瘤组织中常见的现象,由肿瘤细胞和间充质细胞共同调节。细胞外基质中胶原蛋白和赖氨酸氧化酶家族蛋白的增加导致基质的沉积、收缩和交联,促进肿瘤中基质硬度的增加。基质刚度对各种实体瘤的进展至关重要。基质刚度作为肿瘤微环境中的力学因素,参与肿瘤的进展,促进肿瘤细胞增殖、侵袭、转移、血管生成、耐药、免疫逃逸等生物学过程。减少组织僵硬可以减缓肿瘤的进展。因此,靶向基质硬度是肿瘤治疗的潜在选择。本文综述了基质刚度在不同恶性肿瘤表型中的具体机制以及针对基质刚度的潜在肿瘤治疗方法。了解基质刚度在肿瘤中的作用和机制可以为肿瘤的治疗提供理论见解,并有助于新药物治疗的临床开发。
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Matrix stiffness-driven cancer progression and the targeted therapeutic strategy

Increased matrix stiffness is a common phenomenon in solid tumor tissue and is regulated by both tumor and mesenchymal cells. The increase in collagen and lysyl oxidase family proteins in the extracellular matrix leads to deposition, contraction, and crosslinking of the stroma, promoting increased matrix stiffness in tumors. Matrix stiffness is critical to the progression of various solid tumors. As a mechanical factor in the tumor microenvironment, matrix stiffness is involved in tumor progression, promoting biological processes such as tumor cell proliferation, invasion, metastasis, angiogenesis, drug resistance, and immune escape. Reducing tissue stiffness can slow down tumor progression. Therefore targeting matrix stiffness is a potential option for tumor therapy. This article reviews the detailed mechanisms of matrix stiffness in different malignant tumor phenotypes and potential tumor therapies targeting matrix stiffness. Understanding the role and mechanisms of matrix stiffness in tumors could provide theoretical insights into the treatment of tumors and assist in the clinical development of new drug therapies.

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