Comprehensive analysis of expression profiles and prognosis of TRIM genes in human kidney clear cell carcinoma

Abstract

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.

Tripartite motif-containing protein 26 promotes colorectal cancer growth by inactivating p53

“…Furthermore, in Kidney Clear Cell Carcinoma (KIRC) Shen, Wang et al discovered that TRIM26 targets SNRBP, which directly participates in ubiquitination. This study reported shorter lifespan in patients with low levels of TRIM26 ( 22 ).…”

Multi-omics analysis of renal clear cell carcinoma progression

“…For miR-27b, Ishihara et al found that it functions as a tumor suppressor of RCC [42]. Hsa-mir-200b downregulation has been found to suppress metastasis of RCC [43], and hsa-let-7i has been implicated in RCC due to its relationship with TRIM genes [44]. Hsa-mir-24-1 plays a role in several different types of cancer [45] and may be connected to lupus nephritis [46].…”