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:The role of MUC16 in tumor biology and tumor immunology in ovarian cancer.
The role of MUC16 in tumor biology and tumor immunology in ovarian cancer.
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本研究探讨了糖蛋白组学变化,特别是 MUC16,对卵巢癌中 NK 细胞介导的免疫治疗反应的影响。对 CPTAC 数据库中糖蛋白数据的分析发现,MUC16 在卵巢癌组织中显著上调,并与肿瘤侵袭性和免疫逃逸相关。实验结果显示,MUC16 敲低增加了 NK 细胞细胞毒性,降低了侵袭性,并增强了 NK 细胞活化,而 MUC16 过表达则导致相反效果。体内实验表明,MUC16 敲低抑制了肿瘤生长,增强了 NK 细胞浸润,并加强了 NK 细胞活化,凸显了 MUC16 作为卵巢癌治疗中新型免疫治疗方法靶点的潜力。
In this study, the influence of glycoproteomic changes, specifically MUC16, on NK cell-mediated immunotherapy response in ovarian cancer is explored. Analysis of glycoprotein data from the CPTAC database identified significant upregulation of MUC16 in ovarian cancer tissues, associated with tumor invasiveness and immune evasion.
Experimental findings showed that MUC16 knockdown increased NK cell cytotoxicity, decreased invasiveness, and boosted NK cell activation, while MUC16 overexpression resulted in the opposite effects. In vivo experiments demonstrated that MUC16 knockdown suppressed tumor growth, enhanced NK cell infiltration, and bolstered NK cell activation, underscoring the potential of MUC16 as a target for novel immunotherapy approaches in ovarian cancer treatment.
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