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BST2 在人类肿瘤中新兴的致癌与免疫调节作用

英文原题:Emerging Oncogenic and Immunoregulatory Roles of BST2 in Human Cancers.

PubMed 2026/01/08(内容时间) Biomedicines Q2 · IF 4.5(JCR 2025)

研究概要

BST2 是一种双功能分子,整合了致癌信号与免疫调节,使其成为血液系统肿瘤和实体瘤有吸引力的诊断和治疗靶点。

中文摘要

BST2已成为一种多功能分子,连接抗病毒防御、细胞膜结构和肿瘤免疫。BST2最初被描述为干扰素诱导的限制因子,可将病毒颗粒锚定在质膜上;如今被认为是多种恶性肿瘤中的致癌驱动因子和免疫调节枢纽。在癌症中,BST2表达常因启动子低甲基化和转录激活而上调。功能上,BST2促进增殖、上皮—间质转化、失巢凋亡抵抗和化疗耐药;而BST2缺失会使肿瘤细胞对蛋白毒性和代谢应激更加敏感。除肿瘤细胞外,BST2还通过促进M2巨噬细胞浸润、树突状细胞耗竭以及NK细胞耐受来调节肿瘤微环境,从而助长免疫逃逸。胶质母细胞瘤、乳腺癌、鼻咽癌和胰腺癌中BST2高表达与预后不良相关;BST2还可作为小型细胞外囊泡中的循环生物标志物。总之,BST2兼具致癌信号和免疫调控双重功能,是血液系统和实体瘤中有吸引力的诊断及治疗靶点。

展开英文摘要原文

BST2 has emerged as a multifunctional molecule that bridges antiviral defense, membrane architecture, and tumor immunity. Originally characterized as an interferon-inducible restriction factor that tethers virions to the plasma membrane, BST2 is now recognized as an oncogenic driver and immunoregulatory hub in diverse malignancies. In cancer, BST2 expression is frequently upregulated through promoter hypomethylation and transcriptional activation. Functionally, BST2 promotes proliferation, epithelial-mesenchymal transition, anoikis resistance, and chemoresistance, whereas its loss sensitizes tumor cells to proteotoxic and metabolic stresses. Beyond tumor cells, BST2 modulates the tumor microenvironment by promoting M2 macrophage infiltration, dendritic cell exhaustion, and natural killer (NK)-cell resistance, thereby contributing to immune evasion. Elevated BST2 expression correlates with poor prognosis in glioblastoma, breast, nasopharyngeal, and pancreatic cancers, and it serves as a circulating biomarker within small extracellular vesicles. In conclusion, BST2 is a dual-function molecule that integrates oncogenic signaling and immune regulation, making it an attractive diagnostic and therapeutic target for hematological and solid tumors.

论文信息

作者
Kim C、Choi S、Park JW
单位
Department of Health Sciences and Technology, GAIHST, Gachon University, Incheon 21999, Republic of Korea.South Korea
文献类型
综述
期刊
Biomedicines2026 Jan 8
原文标识
PubMed 41595667 · DOI 10.3390/biomedicines14010131