Abstract：
BACKGROUND: Nuclear cap-binding protein 2 (NCBP2), as the component of the cap-binding complex, participates in a number of biological processes, including pre-mRNA splicing, transcript export, translation regulation and other gene expression steps. However, the role of NCBP2 on the tumor cells and immune microenvironment remains unclear. To systematically analyze and validate functions of NCBP2, we performed a pan-cancer analysis using multiple approaches.
METHODS: The data in this study were derived from sequencing, mutation, and methylation data in the TCGA cohort, normal sample sequencing data in the GTEx project, and cell line expression profile data in the CCLE database.
RESULTS: Survival analyses including the Cox proportional-hazards model and log-rank test revealed the poor prognostic role of NCBP2 in multiple tumors. We further validated the oncogenic ability of NCBP2 in prostate cancer cell lines, organoids and tumor-bearing mice. A negative correlation was observed between NCBP2 expression and immune score by the ESTIMATE algorithm. Simultaneously, the NCBP2-induced immunosuppressive microenvironment might be related to the decline in CD8+T cells and the increase in regulatory T cells and neutrophils, examined by flow cytometry experiments for NCBP2 overexpressed tumor-bearing mice.
CONCLUSIONS: This research offered strong proof supporting NCBP2 as the prognostic marker and the therapeutic target in the future.
METHODS: The data in this study were derived from sequencing, mutation, and methylation data in the TCGA cohort, normal sample sequencing data in the GTEx project, and cell line expression profile data in the CCLE database.
RESULTS: Survival analyses including the Cox proportional-hazards model and log-rank test revealed the poor prognostic role of NCBP2 in multiple tumors. We further validated the oncogenic ability of NCBP2 in prostate cancer cell lines, organoids and tumor-bearing mice. A negative correlation was observed between NCBP2 expression and immune score by the ESTIMATE algorithm. Simultaneously, the NCBP2-induced immunosuppressive microenvironment might be related to the decline in CD8+T cells and the increase in regulatory T cells and neutrophils, examined by flow cytometry experiments for NCBP2 overexpressed tumor-bearing mice.
CONCLUSIONS: This research offered strong proof supporting NCBP2 as the prognostic marker and the therapeutic target in the future.
摘要：
背景：核帽结合蛋白2（NCBP2），作为帽结合复合物的组成部分，参与了许多生物过程，包括前mRNA剪接，成绩单导出，翻译调控等基因表达步骤。然而,NCBP2对肿瘤细胞和免疫微环境的作用尚不清楚。为了系统分析和验证NCBP2的功能，我们使用多种方法进行了泛癌症分析。
方法：本研究的数据来自测序，突变,和TCGA队列中的甲基化数据，GTEx项目中的正常样本测序数据，和CCLE数据库中的细胞系表达谱数据。
结果：包括Cox比例风险模型和对数秩检验在内的生存分析显示，NCBP2在多种肿瘤中的预后作用较差。我们进一步验证了NCBP2在前列腺癌细胞系中的致癌能力，类器官和荷瘤小鼠。通过ESTIMATE算法观察到NCBP2表达与免疫评分之间呈负相关。同时,NCBP2诱导的免疫抑制微环境可能与CD8+T细胞减少、调节性T细胞和中性粒细胞增加有关,通过流式细胞术实验检查NCBP2过表达的荷瘤小鼠。
结论：这项研究提供了有力的证据支持NCBP2作为预后标志物和未来的治疗靶点。
方法：本研究的数据来自测序，突变,和TCGA队列中的甲基化数据，GTEx项目中的正常样本测序数据，和CCLE数据库中的细胞系表达谱数据。
结果：包括Cox比例风险模型和对数秩检验在内的生存分析显示，NCBP2在多种肿瘤中的预后作用较差。我们进一步验证了NCBP2在前列腺癌细胞系中的致癌能力，类器官和荷瘤小鼠。通过ESTIMATE算法观察到NCBP2表达与免疫评分之间呈负相关。同时,NCBP2诱导的免疫抑制微环境可能与CD8+T细胞减少、调节性T细胞和中性粒细胞增加有关,通过流式细胞术实验检查NCBP2过表达的荷瘤小鼠。
结论：这项研究提供了有力的证据支持NCBP2作为预后标志物和未来的治疗靶点。
