RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
颗粒酶 B 的促肿瘤作用：机制与治疗意义
英文原题：The pro-tumorigenic roles of granzyme B: mechanisms and therapeutic implications.
查看英文原题
The pro-tumorigenic roles of granzyme B: mechanisms and therapeutic implications.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
中文摘要
颗粒酶B（GZMB）是一种主要由细胞毒性T淋巴细胞（CTLs）和自然杀伤（NK）细胞表达的执行分子。历史上，GZMB表达水平一直作为免疫活性的标志物，指示抗肿瘤免疫的效力。然而，近期证据日益表明，GZMB在肿瘤微环境中也发挥免疫抑制作用。除CTLs和NK细胞外，来源于多种免疫细胞和肿瘤细胞的GZMB通过调控细胞外基质重塑、上皮-间质转化和血管生成等生物学过程，促进肿瘤的发生和进展。本文总结了GZMB的促肿瘤来源及其机制，为其临床意义的全面理解提供依据，以指导更全面的基于GZMB的抗肿瘤治疗。
展开英文摘要原文
Granzyme B (GZMB) is an effector molecule primarily expressed by cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. Historically, GZMB expression levels have served as a marker of immune activity, indicative of the potency of anti-tumor immunity.
However, recent evidence increasingly demonstrates that GZMB also exerts immunosuppressive effects within the tumor microenvironment. Beyond CTLs and NK cells, GZMB derived from multiple immune and tumor cells promotes tumor initiation and progression by regulating biological processes such as extracellular matrix remodeling, epithelial-mesenchymal transition, and angiogenesis.
This paper summarizes the pro-tumor sources and mechanisms of GZMB, providing a comprehensive understanding of its clinical significance to guide more holistic GZMB-based anti-tumor therapies.
论文信息
- 作者
- Zhang Y、Huang H、Xie L、Li C、Zhou X
- 单位
- Department of Thyroid Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou Sichuan, China.China
- 文献类型
- 综述
- 期刊
- Frontiers in immunology2025
- 原文标识
- PubMed 41567188 · DOI 10.3389/fimmu.2025.1733793
在 PubMed 查看 → 出版商原文（DOI） 全文 PDF（PMC）· 可下载 治疗专题与资料阅读指南 资料来源与翻译说明 报告译文或资料问题 →