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Pan-cancer bioinformatics analysis of TIPRL in human tumors
Xuezhong Zhang1, Hao Xue2, Yuanyuan Lv3
1Department of Laboratory Medicine, Zibo Central Hospital, Zibo, Shandong, China.
Introduction:
The 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.
Methods:
TIPRL 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.
Results:
TIPRL 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.
Conclusion:
These findings establish TIPRL as a significant biomarker in cancer progression and immune regulation, warranting further exploration into its therapeutic implications across diverse tumor types.
Insights
The TOR signaling pathway regulator-like (TIPRL) gene is elevated in most cancers and linked to poorer survival, suggesting it's a key biomarker for cancer progression and immune regulation. Further research into TIPRL's therapeutic potential is recommended.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- The TOR signaling pathway regulator-like (TIPRL) gene has a complex role in cancer, but its comprehensive pan-cancer profile is not well understood.
- Investigating TIPRL's expression and function across various cancers is crucial for identifying potential therapeutic targets.
Purpose of the Study:
- To comprehensively analyze the pan-cancer expression profile of TIPRL.
- To investigate the association of TIPRL with patient survival, genetic alterations, immune infiltration, and key cancer-related pathways.
Main Methods:
- Utilized TCGA_GTEx and CPTAC databases for expression and survival analysis.
- Employed GEPIA2, UALCAN, and cBioPortal for expression, alteration, and structural analysis.
- Assessed RNA modifications, immune cell infiltration, tumor mutational burden (TMB), microsatellite instability (MSI), homologous recombination deficiency (HRD), and pathway enrichment using R, STRING, and survival analysis.
Main Results:
- TIPRL expression is upregulated in most cancers, correlating with worse survival in several types (e.g., ACC, BRCA, HNSC).
- Amplifications are the primary genetic alteration of TIPRL, with varied clinical relevance.
- TIPRL shows complex correlations with immune cell infiltration and is associated with genomic instability markers (TMB, MSI, HRD).
- Enrichment analyses indicate TIPRL's involvement in oxidative phosphorylation and autophagy, crucial for tumorigenesis.
Conclusions:
- TIPRL serves as a significant pan-cancer biomarker for prognosis and immune regulation.
- These findings highlight TIPRL as a potential therapeutic target for various cancer types.
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