ArticleNucleic acids research2021
Comprehensive characterization of somatic variants associated with intronic polyadenylation in human cancers.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Whole genome analysis of selection associated with resistance to heat stress in chickens.Scientific reports · 2026Article
- The Function of Poly (U) Binding Splicing Factor 60 (PUF60) in Disease Regulation.Anti-cancer agents in medicinal chemistry · 2026Review
- Article
- Impact of rare non-coding variants on human diseases through alternative polyadenylation outliers.Nature communications · 2025Article
- Review
- Article
- A distinct class of pan-cancer susceptibility genes revealed by an alternative polyadenylation transcriptome-wide association study.Nature communications · 2024Article
- Therapeutic targeting of CPSF3-dependent transcriptional termination in ovarian cancer.Science advances · 2023Article
- The landscape of cryptic antisense transcription in human cancers reveals an oncogenic noncoding RNA in lung cancer.Science advances · 2023Article
- Accurate transcriptome-wide identification and quantification of alternative polyadenylation from RNA-seq data with APAIQ.Genome research · 2023Article
- ipaQTL-atlas: an atlas of intronic polyadenylation quantitative trait loci across human tissues.Nucleic acids research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic single nucleotide variants (SNVs) in cancer genome affect gene expression through various mechanisms depending on their genomic location. While somatic SNVs near canonical splice sites have been reported to cause abnormal splicing of cancer-related genes, whether these SNVs can affect gene expression through other mechanisms remains an open question. Here, we analyzed RNA sequencing and exome data from 4,998 cancer patients covering ten cancer types and identified 152 somatic SNVs near splice sites that were associated with abnormal intronic polyadenylation (IPA). IPA-associated somatic variants favored the localization near the donor splice sites compared to the acceptor splice sites. A proportion of SNV-associated IPA events overlapped with premature cleavage and polyadenylation events triggered by U1 small nuclear ribonucleoproteins (snRNP) inhibition. GC content, intron length and polyadenylation signal were three genomic features that differentiated between SNV-associated IPA and intron retention. Notably, IPA-associated SNVs were enriched in tumor suppressor genes (TSGs), including the well-known TSGs such as PTEN and CDH1 with recurrent SNV-associated IPA events. Minigene assay confirmed that SNVs from PTEN, CDH1, VEGFA, GRHL2, CUL3 and WWC2 could lead to IPA. This work reveals that IPA acts as a novel mechanism explaining the functional consequence of somatic SNVs in human cancer.
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