细胞因子信号转导抑制因子 3 在炎症性肠病及其相关结直肠癌中的作用。

IF 4.2 2区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2024-11-19 DOI:10.1016/j.bbadis.2024.167578

Pengfei Zhang , Bing Pei , Chengxue Yi , Francis Atim Akanyibah , Fei Mao

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引用次数: 0

摘要

炎症性肠病（IBD）和结直肠癌（CRC）作为人类两大肠道疾病，给医学领域带来了挑战。细胞因子信号转导抑制因子 3（SOCS3）是一种通过多种途径负向调节细胞因子信号转导的蛋白质分子，参与调节各种炎症性疾病和肿瘤。在 IBD 中，SOCS3 作用于多种细胞，修复粘膜损伤并平衡免疫反应，包括上皮细胞、巨噬细胞、树突状细胞、中性粒细胞和 T 细胞。在 CRC 中，SOCS3 与肿瘤细胞的增殖、侵袭、转移和耐药性密不可分。因此，系统研究 SOCS3 在 IBD 和 CRC 中的致病参与至关重要。本文综述了 SOCS3 参与抑制 IBD 和缓解 CRC 的机制和途径，并详细介绍了靶向 SOCS3 的治疗方案。

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The role of suppressor of cytokine signaling 3 in inflammatory bowel disease and its associated colorectal cancer

Inflammatory bowel disease (IBD) and colorectal cancer (CRC), as two of the major human intestinal diseases, provide challenges for the medical field. Suppressor of cytokine signaling 3 (SOCS3), a protein molecule that negatively regulates cytokine signaling through multiple pathways, is involved in the regulation of various inflammatory diseases and tumors. In IBD, SOCS3 acts on a variety of cells to repair mucosal damage and balance the immune response, including epithelial cells, macrophages, dendritic cells, neutrophils, and T cells. In CRC, SOCS3 is inextricably linked to tumor cell proliferation, invasion, metastasis, and drug resistance. Therefore, it is crucial to systematically investigate the pathogenic involvement of SOCS3 in IBD and CRC. This article reviews the mechanisms and pathways by which SOCS3 is involved in the inhibition of IBD and the mitigation of CRC, and details the therapeutic options for targeting SOCS3.

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来源期刊

Biochimica et biophysica acta. Molecular basis of disease 生物-生化与分子生物学

CiteScore

12.30

自引率

0.00%

发文量

218

审稿时长

32 days

期刊介绍： BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.