Hery Urra, Raúl Aravena, Lucas González-Johnson, Claudio Hetz
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引用次数: 0
摘要
肿瘤微环境（TME）是由癌细胞、基质细胞、免疫介质和细胞外基质成分组成的动态网络，对癌症的进展至关重要。癌基因激活、营养匮乏和缺氧等应激条件会破坏内质网（ER），激活未折叠蛋白反应（UPR），这是恢复ER功能的主要适应机制。UPR 通过调动细胞自主和细胞非自主机制、重塑基质以及促进免疫逃避、血管生成和侵袭来调控癌症进展。本综述探讨了 UPR 在癌细胞之外的作用，重点关注 ER 应激信号如何重塑 TME，从而支持肿瘤生长。此外，还讨论了针对 UPR 的治疗潜力。
The UPRising connection between endoplasmic reticulum stress and the tumor microenvironment.
The tumor microenvironment (TME) represents a dynamic network of cancer cells, stromal cells, immune mediators, and extracellular matrix components, crucial for cancer progression. Stress conditions such as oncogene activation, nutrient deprivation, and hypoxia disrupt the endoplasmic reticulum (ER), activating the unfolded protein response (UPR), the main adaptive mechanism to restore ER function. The UPR regulates cancer progression by engaging cell-autonomous and cell-non-autonomous mechanisms, reprogramming the stroma and promoting immune evasion, angiogenesis, and invasion. This review explores the role of UPR beyond cancer cells, focusing on how ER stress signaling reshapes the TME, supporting tumor growth. The therapeutic potential of targeting the UPR is also discussed.
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Trends in Cancer, a part of the Trends review journals, delivers concise and engaging expert commentary on key research topics and cutting-edge advances in cancer discovery and medicine.
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