TRIM基因在人肾透明细胞癌中的表达谱及预后综合分析

Junwen Shen, Rong-jiang Wang, Yu Chen, Zhihai Fang, Jian-er Tang, Jianxiang Yao, Jian-guo Gao, Wenxia Zhou, Xiongnong Chen
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引用次数: 2

摘要

目的:探讨TRIM家族基因在肾透明细胞癌(KIRC)中的生存率及其作用机制。方法:从UCSC Xena和GEPIA数据库中检索KIRC患者TRIM基因的转录和生存数据。研究了TRIM基因在KIRC中的功能,重点研究了潜在的泛素化、mirna调控和富集分析。接下来,确定TRIM基因的生存值,然后开发与生存相关的特征。结果:只有TRIM26在癌组织中表达下调,且在KIRC中相对于对照组织具有存活价值,这是体外实验提供的数据。TRIM26表达水平越低,患者生存时间越短。SNRPB也参与泛素化,直接与TRIM26相互作用。此外,还鉴定了两个调节TRIM26表达水平的mirna (hsa-let-7i-5p和hsa-miR-1228-5p)。接下来,我们构建了一个特征(TRIM4/7/27/58/65/72),并发现该特征的高风险评分与KIRC患者的低生存率相关。而其产生的风险评分与免疫细胞成分和标志物相关。结论:TRIM26在KIRC与正常组织中表达存在差异,且在KIRC中具有生存价值。hsa-let-7i-5p/hsa-miR-1228-5p-TRIM26-SNRPB是可能在KIRC细胞中发挥作用的潜在机制轴。成功建立了一个生存特征(TRIM4/7/27/58/65/72)来预测KIRC患者的生存。
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Comprehensive analysis of expression profiles and prognosis of TRIM genes in human kidney clear cell carcinoma
Objective: To determine survival rates and the underlying mechanism of genes in the TRIM family in Kidney Clear Cell Carcinoma (KIRC). Methods: Transcriptional and survival data of TRIM genes in KIRC patients were retrieved from the UCSC Xena, and GEPIA databases. The function of TRIM genes in KIRC was investigated, focusing on potential ubiquitination, miRNAs regulation, and enrichment analysis. Next, TRIM gene survival values were determined, followed by the development of a survival-related signature. Results: Only TRIM26 was down expressed in the carcinoma tissue and had a survival value in KIRC relative to control tissues, which was supplied by vitro experiment. The patients with lower expression of TRIM26 would have the chance to live a shorter time. SNRPB, which also plays a role in ubiquitination, directly interacted with TRIM26. Moreover, two miRNAs (hsa-let-7i-5p, and hsa-miR-1228-5p) that regulated levels of TRIM26 expression were also identified. Next, we constructed a signature (TRIM4/7/27/58/65/72) and found that high-risk scores of the signature were associated with poor survival rates in KIRC patients. while its resultant risk scores were correlated with immune cell components and markers. Conclusions: TRIM26 was differentially expressed between KIRC and normal tissues and had a survival value in the KIRC. hsa-let-7i-5p/hsa-miR-1228-5p-TRIM26-SNRPB was a potential mechanism axis that may play a role on the KIRC cells. A survival signature (TRIM4/7/27/58/65/72) was successfully established to predict the survival of KIRC patients.
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