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
英文原题:Harnessing B7-H6 for Anticancer Immunotherapy: Expression, Pathways, and Therapeutic Strategies.
Harnessing B7-H6 for Anticancer Immunotherapy: Expression, Pathways, and Therapeutic Strategies.
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癌症治疗已从传统化疗发展到更精准的分子靶向免疫治疗,后者与副作用改善和结局改善相关。这些现代策略依赖于能够区分恶性细胞与正常细胞的癌症特异性生物标志物。B7家族免疫检查点分子对癌症免疫逃逸至关重要,也是重要的治疗靶点。B7-H6是近年来发现的B7家族成员,已成为一个有前景的治疗靶点。与其他B7蛋白不同,B7-H6在健康组织中不表达,但在多种癌症中上调。它与NKp30结合,激活自然杀伤(NK)细胞并触发针对癌细胞的免疫反应。本综述探讨了B7-H6在不同癌症中的表达、调控其表达的因素及其内在和外在通路。此外,我们还讨论了靶向B7-H6的潜在抗癌疗法,强调其在推进精准医学中的意义。理解B7-H6在癌症免疫中的作用可能为开发利用其癌症特异性表达的适当疗法提供依据。
Cancer therapies have evolved from traditional chemotherapy to more precise molecular-targeted immunotherapies, which have been associated with improved side effects and outcomes. These modern strategies rely on cancer-specific biomarkers that differentiate malignant from normal cells. The B7 family of immune checkpoint molecules is crucial for cancer immune evasion and a prime therapeutic target.
B7-H6, a recently identified member of the B7 family, has emerged as a promising therapeutic target. Unlike other B7 proteins, B7-H6 is not expressed in healthy tissues but is upregulated in several cancers. It binds to NKp30, activating natural killer (NK) cells and triggering immune responses against cancer cells. This review explores the expression of B7-H6 in different cancers, the factors that regulate its expression, and its intrinsic and extrinsic pathways.
Additionally, we discuss potential anticancer therapies targeting B7-H6, highlighting its significance in advancing precision medicine. Understanding the role of B7-H6 in cancer immunity may inform the development of appropriate therapies that exploit its cancer-specific expression.
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