TP53 缺失通过上调 NF-κB-IFN-β-MHC-Ia 信号促进骨肉瘤对 NK 细胞的抵抗
TP53 Loss Elevates NF-κB-IFN-β-MHC-Ia Signaling to Promote NK Cell Resistance in Osteosarcoma.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Microenvironment plays a critical role in modulating tumor cell dormancy: Current perspectives and potential treatment options.
Microenvironment plays a critical role in modulating tumor cell dormancy: Current perspectives and potential treatment options.
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肿瘤休眠是肿瘤生物学中的一个基本现象,其特征是恶性细胞保持存活但不再增殖,从而常常逃避检测和治疗。本综述探讨了肿瘤微环境(TME)在调控肿瘤细胞休眠中的复杂作用。TME包含多种多样的组分,包括免疫细胞、细胞外基质蛋白和可溶性因子,这些组分共同构成了影响肿瘤细胞行为的动态相互作用。参与维持休眠的关键机制包括免疫监视,其中免疫细胞既可抑制也可促进肿瘤生长,以及细胞外基质相互作用,后者提供静息状态所必需的结构支持和生化信号。
此外,缺氧和酸中毒等微环境条件施加选择压力,可有利于休眠状态而非活跃增殖。目前正在探索针对休眠肿瘤细胞的新兴治疗策略,包括使用间充质干细胞疗法,该疗法可能调节TME以唤醒休眠细胞进行靶向治疗,或维持其静息状态以防止复发。理解TME对肿瘤休眠的影响不仅增强了我们对肿瘤进展的认识,还开辟了创新治疗途径,旨在通过降低复发和转移风险来改善患者预后。本文旨在全面概述当前关于TME介导的肿瘤休眠的知识,并强调未来研究中有前景的治疗策略。
Tumor dormancy is a fundamental phenomenon in cancer biology, characterized by malignant cells that remain viable but non-proliferative, thereby frequently evading detection and treatment. This review examines the intricate role of the tumor microenvironment (TME) in regulating tumor cell dormancy.
The TME encompasses a diverse array of components, including immune cells, extracellular matrix proteins, and soluble factors, all of which contribute to a dynamic interplay that influences tumor cell behavior. Key mechanisms involved in the maintenance of dormancy include immune surveillance, where immune cells can either suppress or promote tumor growth, and extracellular matrix interactions that provide structural support and biochemical signals essential for quiescence.
Additionally, microenvironmental conditions such as hypoxia and acidosis impose selective pressures that can favor dormant states over active proliferation. Emerging therapeutic strategies are being explored to target dormant tumor cells, including the use of mesenchymal stem cell therapies, which may modulate the TME to either awaken dormant cells for targeted treatment or maintain their quiescent state to prevent recurrence.
Understanding the TME's influence on tumor dormancy not only enhances our comprehension of cancer progression but also opens avenues for innovative treatments aimed at improving patient outcomes by mitigating the risks of recurrence and metastasis. This article aims to provide a comprehensive overview of the current knowledge on TME-mediated tumor dormancy and highlight promising therapeutic strategies for future research.
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