结直肠癌（CRC）仍然是一个重大的全球健康挑战，其特点是近年来发病率和死亡率不断上升。 CRC的发病机制复杂，涉及肠粘膜的慢性炎症、免疫炎症反应增强和细胞凋亡抵抗。细胞因子信号传导抑制因子 (SOCS) 家族由细胞因子信号传导途径中的关键负调节因子组成，在细胞增殖、生长和代谢调节中发挥着至关重要的作用。各种 SOCS 蛋白的缺陷可在细胞因子和生长因子与其受体结合后触发 Janus 激酶 (JAK) 以及信号转导子和转录激活子 (STAT) 途径的激活。越来越多的证据表明，SOCS 蛋白是结直肠癌发生和进展不可或缺的一部分，这使它们成为新型抗癌疗法的有希望的靶点。这篇综述深入研究了 SOCS 家族成员的结构、功能和分子机制，研究了它们在细胞增殖、凋亡、迁移、上皮间质转化 (EMT) 和免疫调节中的作用。此外，它还探讨了它们对 CRC 免疫治疗监管的潜在影响，提供了新的见解和观点，可以为 CRC 创新治疗策略的开发提供信息。版权所有 © 2024 Elsevier GmbH。版权所有。

Colorectal cancer (CRC) remains a significant global health challenge, marked by increasing incidence and mortality rates in recent years. The pathogenesis of CRC is complex, involving chronic inflammation of the intestinal mucosa, heightened immunoinflammatory responses, and resistance to apoptosis. The suppressor of cytokine signaling (SOCS) family, comprised of key negative regulators within cytokine signaling pathways, plays a crucial role in cell proliferation, growth, and metabolic regulation. Deficiencies in various SOCS proteins can trigger the activation of the Janus kinase (JAK) and signal transducers and activators of transcription (STAT) pathways, following the binding of cytokines and growth factors to their receptors. Mounting evidence indicates that SOCS proteins are integral to the development and progression of CRC, positioning them as promising targets for novel anticancer therapies. This review delves into the structure, function, and molecular mechanisms of SOCS family members, examining their roles in cell proliferation, apoptosis, migration, epithelial-mesenchymal transition (EMT), and immune modulation. Additionally, it explores their potential impact on the regulation of CRC immunotherapy, offering new insights and perspectives that may inform the development of innovative therapeutic strategies for CRC.Copyright © 2024 Elsevier GmbH. All rights reserved.