Abstract
pre-mRNA processing factor 3 (PRPF3) is an RNA binding protein in a core component of the exon junction complex. Abnormal PRPF3 expression is potentially associated with carcinogenesis. However, the biological role of PRPF3 in hepatocellular carcinoma (HCC) remains to be determined. We analyzed PRPF3 expression via multiple gene expression databases and identified its genetic alterations and functional networks using cBioPortal. Co-expressed genes with PRPF3 and its regulators were identified using LinkedOmics. The correlations between PRPF3 and cancer immune infiltrates were investigated via Tumor Immune Estimation Resource (TIMER). PRPF3 was found up-regulated with amplification in tumor tissues in multiple HCC cohorts. High PRPF3 expression was associated with poorer overall survival (OS) and disease-free survival (DFS). Functional network analysis suggested that PRPF3 regulates spliceosome, DNA replication, and cell cycle signaling via pathways involving several cancer-related kinases and E2F family. Notably, PRPF3 expression was positively correlated with infiltrating levels of CD4+ T and CD8+ T cells, macrophages, neutrophils, and dendritic cells. PRPF3 expression showed strong correlations with diverse immune marker sets in HCC. These findings suggest that PRPF3 is correlated with prognosis and immune infiltrating in HCC, laying a foundation for further study of the immune regulatory role of PRPF3 in HCC.
Highlights
Hepatocellular carcinoma (HCC) is the most common form of liver cancers [1], which has an annual incidence of at least 6 per 100,000 individuals and represents the fastest-rising cause of cancer-related death [2]
We initially evaluated pre-mRNA processing factor 3 (PRPF3) transcription levels in multiple hepatocellular carcinoma (HCC) studies from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO)
Data in the Oncomine database indicated that PRPF3 ranked within the top 10% based on mRNA expression (Figure 1B)
Summary
Hepatocellular carcinoma (HCC) is the most common form of liver cancers [1], which has an annual incidence of at least 6 per 100,000 individuals and represents the fastest-rising cause of cancer-related death [2]. Existing targeted drugs show unsatisfactory efficacy, due to a combination of factors spanning an array of different clinical and biological behaviors, and the development of anti-HCC drug resistance [3]. The molecular mechanisms underlying tumor formation and progression are poorly understood, which further complicates the effective treatment of HCC [4]. The lack of markers that are specific for tumor type or disease stage represents a critical gap in the current understanding and treatment of HCC. Pre-mRNA splicing is a fundamental process that plays a considerable role in generating protein diversity. Prewww.aging-us.com mRNA splicing is the key to the pathology of numerous diseases, especially cancers [5]. The connection between cancer biology and splicing regulation is of primary importance to understand the mechanisms leading to disease and to improve the development of therapeutic approaches [6]. Among the array of splicing factors, pre-mRNA processing factor 3 (PRPF3), a component of the U4/U6 di-snRNP, is required for U4/U6U5 tri-snRNP formation and recruitment to active spliceosomes, which is essential for efficient pre-mRNA splicing [7, 8]
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