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:Integrated multi-omics analysis of UL16-binding protein 2 as a prognostic and immunotherapy biomarker for colorectal cancer.
Integrated multi-omics analysis of UL16-binding protein 2 as a prognostic and immunotherapy biomarker for colorectal cancer.
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ULBP2 有潜力作为 CRC 的预后生物标志物和治疗靶点。这些发现为未来肿瘤发生机制和临床应用的研究提供了有价值的见解。
UL16结合蛋白2(ULBP2)是一种重要的免疫调节分子,参与NK 细胞活化和肿瘤免疫监视,但其在结直肠癌(CRC)中的具体作用及临床意义仍需进一步探索。
通过癌症基因组图谱和基因表达综合数据库分析ULBP2在CRC与正常组织中的表达,以及其与临床病理特征的潜在关联,同时使用受试者工作特征(ROC)曲线评估诊断价值,并通过Kaplan-Meier和Cox回归分析评估预后影响。此外,通过研究启动子DNA甲基化、m6A调控和免疫细胞浸润,探索ULBP2的调控机制。最后,进行细胞实验以评估ULBP2作为预测CRC进展的潜在生物标志物。
ULBP2上调与CRC晚期病理分期显著相关。ROC曲线分析表明ULBP2具有较强的诊断价值。Kaplan-Meier生存分析显示,ULBP2高表达预示预后较差。Cox回归分析突出表明ULBP2是一个独立预后因素。ULBP2表达与启动子甲基化、m6A调控和免疫细胞浸润相关。细胞实验表明,敲低ULBP2可抑制CRC进展。
UL16-binding protein 2 (ULBP2) is an important immune regulatory molecule involved in natural killer cell activation and tumor immune surveillance, although the specific role and clinical significance in colorectal cancer (CRC) require further exploration.
ULBP2 expression in CRC vs. normal tissues was analyzed using The Cancer Genome Atlas and the Gene Expression Omnibus databases, along with potential associations with clinicopathological features, while the diagnostic value was assessed with receiver operating characteristic (ROC) curves and the prognostic impact by Kaplan-Meier and Cox regression analyses. Additionally, the regulatory mechanisms of ULBP2 were explored by investigations of promoter DNA methylation, m6A regulation, and immune cell infiltration. Finally, cellular experiments were conducted to evaluate ULBP2 as a potential biomarker to predict CRC progression.
ULBP2 upregulation was significantly correlated with an advanced pathological stage of CRC. ROC curve analysis indicated that ULBP2 has strong diagnostic value. Kaplan-Meier survival analysis showed that high ULBP2 expression was predictive of a poorer prognosis. Cox regression analysis highlighted ULBP2 as an independent prognostic factor. ULBP2 expression was linked to promoter methylation, m6A regulation, and immune cell infiltration. Cellular experiments showed that ULBP2 knockdown suppressed CRC progression.
ULBP2 has potential as a prognostic biomarker and therapeutic target of CRC. These findings provide valuable insights for future studies of tumorigenic mechanisms and clinical applications.
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