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SNRPB2 in the pan-cancer landscape: A bioinformatics exploration and validation in hepatocellular carcinoma
Bowen Li1, Jiang Liu2, Ling Huang3
1Department of Interventional and Vascular Surgery, Affiliated Hospital of Jinggangshan University, Ji'an 343009, Jiangxi Province, China; Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330000, Jiangxi Province, China.
Abstract:
Aberrant splicing is a significant contributor to gene expression abnormalities in cancer. SNRPB2, a component of U2 small nuclear ribonucleoprotein particles (snRNPs), contributes to the assembly of the spliceosome, the molecular machinery responsible for splicing. To date, few studies have investigated the role of SNRPB2 in tumorigenesis. We examined data sourced from various public databases, such as The Cancer Genome Atlas(TCGA), the Clinical Proteomic Tumor Analysis Consortium(CPTAC), and Gene Expression Omnibus(GEO). Our investigation included gene expression, genomic and epigenomic scrutiny, gene set enrichment assessment(GSEA), and immune cell infiltration evaluation. Furthermore, we performed empirical validation to ascertain the impact of SNRPB2 suppression on the proliferation and migration of liver cancer cells. Analysis of gene expression revealed widespread upregulation of SNRPB2 across a spectrum of cancer types, with heightened levels of SNRPB2 expression in numerous tumors linked to unfavorable prognosis. Genomic and epigenomic assessments revealed connections between SNRPB2 expression and variations in SNRPB2 copy number, DNA methylation patterns, and RNA modifications. Through gene set enrichment analysis, the involvement of SNRPB2 in vital biological processes and pathways related to cancer was identified. Furthermore, scrutiny of immune cell infiltration suggested a potential relationship between SNRPB2 and the tumor microenvironment, which was reinforced by multiple single-cell sequencing profiles. Subsequent experimental validation revealed that silencing SNRPB2 effectively impeded the proliferation and migration of liver cancer cells. Taken together, these findings underscore the prospective utility of SNRPB2 as a prognostic biomarker and a promising candidate for immunotherapy in cancer. It is necessary to engage in additional exploration into its underlying mechanisms and clinical treatment potential.
Insights
SNRPB2, a spliceosome component, is upregulated in many cancers and linked to poor prognosis. Suppressing SNRPB2 inhibits liver cancer cell growth and migration, suggesting its potential as a cancer biomarker and therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Aberrant splicing contributes to cancer gene expression abnormalities.
- SNRPB2 (snRNP core protein B2) is crucial for spliceosome assembly.
- Its role in tumorigenesis remains largely unexplored.
Purpose of the Study:
- Investigate the role of SNRPB2 in cancer development and progression.
- Evaluate SNRPB2 as a prognostic biomarker and potential therapeutic target.
Main Methods:
- Analysis of public databases (TCGA, CPTAC, GEO) for gene expression, genomics, and epigenomics.
- Gene Set Enrichment Analysis (GSEA) and immune cell infiltration analysis.
- Experimental validation of SNRPB2 suppression in liver cancer cells.
Main Results:
- SNRPB2 is upregulated across various cancers, correlating with unfavorable prognosis.
- SNRPB2 expression is linked to genomic alterations (copy number, methylation, RNA modifications).
- SNRPB2 silencing inhibits liver cancer cell proliferation and migration, and is associated with tumor microenvironment factors.
Conclusions:
- SNRPB2 is a potential prognostic biomarker in cancer.
- SNRPB2 represents a promising target for cancer immunotherapy.
- Further research is needed to elucidate SNRPB2's mechanisms and clinical applications.
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