Abstract：
The intrinsic oncogenic mechanisms and properties of the tumor microenvironment (TME) have been extensively investigated. Primary features of the TME include metabolic reprogramming, hypoxia, chronic inflammation, and tumor immunosuppression. Previous studies suggest that senescence-associated secretory phenotypes that mediate intercellular information exchange play a role in the dynamic evolution of the TME. Specifically, hypoxic adaptation, metabolic dysregulation, and phenotypic shifts in immune cells regulated by cellular senescence synergistically contribute to the development of an immunosuppressive microenvironment and chronic inflammation, thereby promoting the progression of tumor events. This review provides a comprehensive summary of the processes by which cellular senescence regulates the dynamic evolution of the tumor-adapted TME, with focus on the complex mechanisms underlying the relationship between senescence and changes in the biological functions of tumor cells. The available findings suggest that components of the TME collectively contribute to the progression of tumor events. The potential applications and challenges of targeted cellular senescence-based and combination therapies in clinical settings are further discussed within the context of advancing cellular senescence-related research.
摘要：
肿瘤微环境（TME）的内在致癌机制和特性已得到广泛研究。TME的主要特征包括代谢重编程，缺氧,慢性炎症，和肿瘤免疫抑制。先前的研究表明，介导细胞间信息交换的衰老相关分泌表型在TME的动态进化中起作用。具体来说,低氧适应,代谢失调,和细胞衰老调节的免疫细胞的表型变化协同促进免疫抑制微环境和慢性炎症的发展，从而促进肿瘤事件的进展。这篇综述提供了细胞衰老调节肿瘤适应TME动态进化的过程的全面总结。重点研究衰老与肿瘤细胞生物学功能变化之间关系的复杂机制。现有的发现表明，TME的成分共同促进了肿瘤事件的进展。在推进细胞衰老相关研究的背景下，进一步讨论了基于靶向细胞衰老和联合治疗在临床环境中的潜在应用和挑战。
