About IPAfunc

Intronic polyadenylation (IpA) sites are shown to generate tumor-specific transcripts and play critical roles in tumor progression. Unlike alternative polyadenylation at 3'UTR, IpA occurs within the introns of genes, leading to a stop in normal transcription and producing truncated mRNA isoforms that can generate dysfunctional proteins or noncoding RNAs. IpA is commonly observed in cancer cells and contributes to the inactivation of DNA damage repair genes and tumor suppressors. However, the potential roles and clinical implications of IpAs in human cancers remain poorly understood. To gain a comprehensive understanding of IpA, we have developed a knowledgebase called IPAfunc. This database is designed to provide functional annotations and clinical relevance of IpAs across various cancer types. Based on three major resources (TCGA, CPTAC, and CCLE), we perform comprehensive analysis, including the effects of IpAs on alternative splicing, miRNA binding, and RBP regulation, as well as the regulatory mechanisms of IpAs, including IpA quantitative trait methylation (IpA-QTM) and single-nucleotide variants (SNVs). Notably, we undertake a systematic investigation into the clinical significance of IpAs, including the characterization of IpAs associated with tumor stage and patient survival, exploration of IpAs linked to immune infiltration, and identification of IpAs contributing to drug resistance.