Pan-cancer bioinformatics analysis of TIPRL in human tumors.

introductionThe TOR signaling pathway regulator-like (TIPRL) gene plays a multifaceted role in cancer, yet its pan-cancer profile remains underexplored. This study investigates TIPRL expression across multiple cancers and its associations with survival, genetic alterations, immune infiltration, and functional pathways, providing insights into TIPRL's role as a potential prognostic and therapeutic target.

methodsTIPRL expression and prognostic significance across tumor types were analyzed using TCGA_GTEx and CPTAC data in R software and platforms like GEPIA2 and UALCAN. Genetic alterations and 3D structures were evaluated through cBioPortal. Associations with RNA modifications, immune checkpoints, immune cell infiltration, TMB, MSI, HRD, and enriched pathways were assessed via R and STRING databases, employing survival analysis, ssGSEA, and enrichment analyses.

resultsTIPRL expression was elevated in most cancers, with significant stage-specific associations observed in KICH, KIRP, and LUSC. High TIPRL expression correlated with worse overall survival in ACC, BRCA, HNSC, KICH, LIHC, and MESO, suggesting its role in prognosis. Genetic analysis identified amplifications as the main alteration, with varied clinical relevance across cancers. RNA modifications in TIPRL, particularly m1A, m5C, and m6A, suggested potential regulatory mechanisms. Immune infiltration analysis revealed TIPRL's varied correlations with immune cell types and immune scores, differing by cancer type. TIPRL also positively correlated with TMB, MSI, and HRD in several cancers, indicating its association with genomic instability. Enrichment analyses highlighted TIPRL's involvement in processes like oxidative phosphorylation and autophagy, underscoring its influence in tumorigenesis.

conclusionThese findings establish TIPRL as a significant biomarker in cancer progression and immune regulation, warranting further exploration into its therapeutic implications across diverse tumor types.