内质网应激（ERS）是一种以内质网（ER）过度收缩为特征的细胞应激反应。它是许多疾病的病理标志，例如糖尿病、肥胖症和神经退行性疾病。在癌症独特的生长特性和多样的微环境中，高水平的应激是维持肿瘤细胞快速增殖和转移所必需的。这一过程与ERS密切相关，ERS增强肿瘤细胞适应不利环境的能力，促进癌症的恶性进展。本文综述了ERS在肿瘤细胞增殖、凋亡、转移、血管生成、耐药、细胞代谢和免疫反应中的作用和机制。我们发现 ERS ​​可以通过 IRE1、PERK 和 ATF6 的未折叠蛋白反应 (UPR) 信号调节肿瘤进展。针对 ERS ​​可能是减弱 ERS ​​对癌症保护作用的新策略。这篇手稿探讨了 ERS ​​靶向治疗的潜力，详细介绍了 ERS ​​影响癌症进展的机制，并强调了支持这些策略的实验和临床证据。通过这次综述，我们旨在加深对 ER 应激在癌症发展中的作用的理解，并为癌症治疗提供新的见解。© 2024。作者。

Endoplasmic reticulum stress (ERS) is a cellular stress response characterized by excessive contraction of the endoplasmic reticulum (ER). It is a pathological hallmark of many diseases, such as diabetes, obesity, and neurodegenerative diseases. In the unique growth characteristic and varied microenvironment of cancer, high levels of stress are necessary to maintain the rapid proliferation and metastasis of tumor cells. This process is closely related to ERS, which enhances the ability of tumor cells to adapt to unfavorable environments and promotes the malignant progression of cancer. In this paper, we review the roles and mechanisms of ERS in tumor cell proliferation, apoptosis, metastasis, angiogenesis, drug resistance, cellular metabolism, and immune response. We found that ERS can modulate tumor progression via the unfolded protein response (UPR) signaling of IRE1, PERK, and ATF6. Targeting the ERS may be a new strategy to attenuate the protective effects of ERS on cancer. This manuscript explores the potential of ERS-targeted therapies, detailing the mechanisms through which ERS influences cancer progression and highlighting experimental and clinical evidence supporting these strategies. Through this review, we aim to deepen our understanding of the role of ER stress in cancer development and provide new insights for cancer therapy.© 2024. The Author(s).