Figure - available from: Human Genomics
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Survival analysis and immune infiltration analysis between high-risk and low-risk groups. (A) The risk score, survival time and expression level of hub genes in high-risk and low-risk groups in all samples. (B) K-M analysis between high-risk and low-risk groups. (C) The risk score of TRIM cluster A was higher than TRIM cluster B. (D) The Sankey diagram displayed the distribution of the samples after twice consensus clustering analysis and risk score construction, as well as survival outcomes. (E) Stromal score, immune score and ESTIMATE score in high-risk and low-risk groups. (F) The correlation analysis in CD4 + memory T cells, mast cells and Tfh with risk score. R referred as the correlation coefficient. ns, p ≥ 0.05; *p < 0.05; **p < 0.01; ***p < 0.001
Source publication
Most TRIM family members characterized by the E3-ubiquitin ligases, participate in ubiquitination and tumorigenesis. While there is a dearth of a comprehensive investigation for the entire family in gastric cancer (GC). By combining the TCGA and GEO databases, common TRIM family members (TRIMs) were obtained to investigate gene expression, gene mut...
Citations
... Additionally, several TRIM proteins, including TRIM15, TRIM47, and TRIM55, have been implicated in EMT. These proteins facilitate EMT by modulating key molecular markers such as E-cadherin, N-cadherin, and Vimentin, contributing to increased cancer cell invasiveness and metastatic potential [74][75][76]145,[151][152][153][154][155][156][157][158][159]. ...
Tripartite motif (TRIM) family proteins, distinguished by their N-terminal region that includes a Really Interesting New Gene (RING) domain with E3 ligase activity, two B-box domains, and a coiled-coil region, have been recognized as significant contributors in carcinogenesis, primarily via the ubiquitin–proteasome system (UPS) for degrading proteins. Mechanistically, these proteins modulate a variety of signaling pathways, including Wnt/β-catenin, PI3K/AKT, and TGF-β/Smad, contributing to cellular regulation, and also impact cellular activities through non-signaling mechanisms, including modulation of gene transcription, protein degradation, and stability via protein–protein interactions. Currently, growing evidence indicates that TRIM proteins emerge as potential regulators in gastric cancer, exhibiting both tumor-suppressive and oncogenic roles. Given their critical involvement in cellular processes and the notable challenges of gastric cancer, exploring the specific contributions of TRIM proteins to this disease is necessary. Consequently, this review elucidates the roles and mechanisms of TRIM proteins in gastric cancer, emphasizing their potential as therapeutic targets and prognostic factors.
