文章：

内质网应激在癌症中的致瘤与免疫抑制作用

Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer

原文发布日期：2017-02-09

DOI: 10.1016/j.cell.2016.12.004

类型: Review

开放获取: 是

英文摘要：

Malignant cells utilize diverse strategies that enable them to thrive under adverse conditions while simultaneously inhibiting the development of anti-tumor immune responses. Hostile microenvironmental conditions within tumor masses, such as nutrient deprivation, oxygen limitation, high metabolic demand, and oxidative stress, disturb the protein-folding capacity of the endoplasmic reticulum (ER), thereby provoking a cellular state of “ER stress.” Sustained activation of ER stress sensors endows malignant cells with greater tumorigenic, metastatic, and drug-resistant capacity. Additionally, recent studies have uncovered that ER stress responses further impede the development of protective anti-cancer immunity by manipulating the function of myeloid cells in the tumor microenvironment. Here, we discuss the tumorigenic and immunoregulatory effects of ER stress in cancer, and we explore the concept of targeting ER stress responses to enhance the efficacy of standard chemotherapies and evolving cancer immunotherapies in the clinic.

摘要翻译： 

恶性细胞利用多种策略使它们能够在不利条件下生存，同时抑制抗肿瘤免疫反应的发展。肿瘤内部恶劣的微环境条件，如营养匮乏、氧气限制、高代谢需求和氧化应激，干扰了内质网的蛋白质折叠能力，从而引发细胞的"内质网应激"状态。内质网应激传感器的持续激活赋予恶性细胞更强的致瘤性、转移性和耐药能力。此外，近期研究发现，内质网应激反应还能通过调控肿瘤微环境中髓样细胞的功能，进一步阻碍保护性抗癌免疫的发展。本文探讨了内质网应激在癌症中的致瘤作用及免疫调节效应，并探索了靶向内质网应激反应以提升标准化疗和新兴癌症免疫疗法临床疗效的策略。

原文链接：

Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer