Comprehensive analysis of TRIM56’s prognostic value and immune infiltration in Pan-Cancer

Abstract

TRIM56 plays a role in tumor development through the ubiquitination of several key substrate molecules. However, its relationship with tumor prognosis and immune infiltration remains unclear. The expression and localization of TRIM56 were analyzed from TCGA_GTEx, TCGA and HPA database. The effects of TRIM56 on the proliferation and migration of lung cancer cells A549 were evaluated by CCK-8 and wound healing assays. Correlations between TRIM56 expression and survival in patients were analyzed using the Kaplan-Meier Plotter and a nomogram model. Additionally, the relationship between TRIM56 and immune cell infiltration in tumors was explored via TIMER 2.0. Functional interactions and associated proteins of TRIM56 were examined using GEPIA 2.0 and the STING database. The signaling pathways influenced by TRIM56 were identified through GO and KEGG analyses. TRIM56 expression showed significant variation across 11 different tumor types when compared to normal tissues, with some tumors displaying high expression and others showing the opposite. TRIM56 inhibited the proliferation and migration of A549 cells. High TRIM56 expression was associated with shorter overall survival (OS) in patients with COAD, GBM, and LGG, but with longer OS in BLCA, KIRC, MESO, and SKCM. In BLCA and KIRC, high TRIM56 expression was closely linked to B cells, macrophages, and CD4(+) and CD8(+) T cell infiltration, contributing to a favorable prognosis. TRIM56 appears to affect tumor development through transcriptional regulatory complexes, transcriptional co-regulatory factor activity, and immune-related pathways.TRIM56 may play a critical role in tumor immunity and influence tumor prognosis. It holds potential as both a target for immunotherapy and a prognostic marker.