内质网应激的致癌性和免疫抑制效应

Tumorigenicity and Immunosuppressive Effects of Endoplasmic Reticulum

不利的肿瘤微环境（tumor microenvironment,TME）会干扰内质网（endoplasmic reticulum,ER）的蛋白折叠,引发内质网应激（endoplasmic reticulum stress,ERS）。持续ERS使肿瘤细胞有更大的致癌性、转移性和耐药性。此外,ERS通过控制TME中骨髓细胞的功能抑制抗癌免疫。全文综述ERS的致瘤性和免疫调节作用,探索靶向ERS反应,以期开展新型的肿瘤免疫疗法。

Hostile microenvironmental conditions of tumor may disturb the protein-folding capacity of the endoplasmic reticulum（ER）,thereby provoking a cellular state of endoplasmic reticulum stress（ERS）. Sustained activation of ERS endows cancer cells with greater malignant,metastatic,and drug-resistant capacity. Additionally,ERS responses can impede the development of anti-cancer immunity by manipulating the function of myeloid cells in the tumor microenvironment. Here,we discuss the tumorigenic and immunoregulatory effects of ERS in cancer cells,and explore the novel strategy to enhance chemotherapy and immunotherapy with ER stress responses as the therapeutic target.