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结直肠癌肝转移中的免疫调节分子。

Immunomodulatory molecules in colorectal cancer liver metastasis.

机构信息

Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, China; Research Unit of Precision Diagnosis and Treatment for Gastrointestinal Cancer, Chinese Academy of Medical Sciences, Guangzhou, 510060, China.

Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, China.

出版信息

Cancer Lett. 2024 Aug 28;598:217113. doi: 10.1016/j.canlet.2024.217113. Epub 2024 Jul 14.

DOI:10.1016/j.canlet.2024.217113
PMID:39009068
Abstract

Colorectal cancer (CRC) ranks as the third most common cancer and the second leading cause of cancer-related deaths. According to clinical diagnosis and treatment, liver metastasis occurs in approximately 50 % of CRC patients, indicating a poor prognosis. The unique immune tolerance of the liver fosters an immunosuppressive tumor microenvironment (TME). In the context of tumors, numerous membrane and secreted proteins have been linked to tumor immune evasion as immunomodulatory molecules, but much remains unknown about how these proteins contribute to immune evasion in colorectal cancer liver metastasis (CRLM). This article reviews recently discovered membrane and secreted proteins with roles as both immunostimulatory and immunosuppressive molecules within the TME that influence immune evasion in CRC primary and metastatic lesions, particularly their mechanisms in promoting CRLM. This article also addresses screening strategies for identifying proteins involved in immune evasion in CRLM and provides insights into potential protein targets for treating CRLM.

摘要

结直肠癌(CRC)位居第三大常见癌症之列,也是癌症相关死亡的第二大主要原因。根据临床诊断和治疗,约 50%的 CRC 患者发生肝转移,预示着预后不良。肝脏独特的免疫耐受促进了免疫抑制性肿瘤微环境(TME)。在肿瘤中,许多膜和分泌蛋白已被确定为具有免疫调节功能的分子,可逃避肿瘤免疫,但这些蛋白如何促进结直肠癌肝转移(CRLM)中的免疫逃避仍知之甚少。本文综述了最近发现的具有免疫刺激和免疫抑制分子作用的膜和分泌蛋白,这些蛋白在 TME 中影响 CRC 原发和转移病变中的免疫逃避,特别是它们在促进 CRLM 中的机制。本文还讨论了用于鉴定 CRLM 中免疫逃避相关蛋白的筛选策略,并为治疗 CRLM 提供了潜在的蛋白靶点。

相似文献

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Immunomodulatory molecules in colorectal cancer liver metastasis.结直肠癌肝转移中的免疫调节分子。
Cancer Lett. 2024 Aug 28;598:217113. doi: 10.1016/j.canlet.2024.217113. Epub 2024 Jul 14.
2
Highly-metastatic colorectal cancer cell released miR-181a-5p-rich extracellular vesicles promote liver metastasis by activating hepatic stellate cells and remodelling the tumour microenvironment.高转移性结直肠癌细胞释放富含 miR-181a-5p 的细胞外囊泡通过激活肝星状细胞和重塑肿瘤微环境促进肝转移。
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Mucosa-associated invariant T cells infiltrate hepatic metastases in patients with colorectal carcinoma but are rendered dysfunctional within and adjacent to tumor microenvironment.黏膜相关恒定T细胞浸润于结直肠癌患者的肝转移灶中,但在肿瘤微环境内及周边会发生功能障碍。
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Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis.结直肠癌发病机制和肝转移中的免疫逃逸机制。
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Cancer-associated stroma reveals prognostic biomarkers and novel insights into the tumour microenvironment of colorectal cancer and colorectal liver metastases.癌症相关基质揭示了结直肠癌和结直肠肝转移瘤肿瘤微环境的预后生物标志物和新见解。
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Tumor-derived exosomal miR-934 induces macrophage M2 polarization to promote liver metastasis of colorectal cancer.肿瘤来源的外泌体 miR-934 诱导巨噬细胞 M2 极化促进结直肠癌肝转移。
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Single-cell transcriptome analysis reveals tumor immune microenvironment heterogenicity and granulocytes enrichment in colorectal cancer liver metastases.单细胞转录组分析揭示结直肠癌肝转移瘤肿瘤免疫微环境异质性和粒细胞富集。
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Unveiling the immune symphony: decoding colorectal cancer metastasis through immune interactions.揭示免疫的交响乐:通过免疫相互作用解码结直肠癌转移。
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Mechanisms of colorectal liver metastasis development.结直肠癌肝转移发展的机制。
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Neutrophil Extracellular Traps Promote T Cell Exhaustion in the Tumor Microenvironment.中性粒细胞胞外陷阱促进肿瘤微环境中的 T 细胞耗竭。
Front Immunol. 2021 Nov 24;12:785222. doi: 10.3389/fimmu.2021.785222. eCollection 2021.

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The Impact of Tertiary Lymphoid Structures on Tumor Prognosis and the Immune Microenvironment in Colorectal Cancer.
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Biomedicines. 2025 Feb 21;13(3):539. doi: 10.3390/biomedicines13030539.
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World J Clin Oncol. 2025 Mar 24;16(3):101725. doi: 10.5306/wjco.v16.i3.101725.
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Front Oncol. 2025 Feb 5;15:1525280. doi: 10.3389/fonc.2025.1525280. eCollection 2025.
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