ArticleGenome research2020
Alternative polyadenylation drives oncogenic gene expression in pancreatic ductal adenocarcinoma.
Article in Genome research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 79 citations in OpenAlex.
- Mechanisms of transcription termination across the coding and noncoding loci of the genome.Nature reviews. Molecular cell biology · 2026Review
- SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma.Genes & diseases · 2025Article
- Transcriptome-wide association study of alternative polyadenylation identifies susceptibility genes in non-small cell lung cancer.Oncogene · 2025Article
- Article
- The CFII components PCF11 and Cbc change subnuclear localization as cells differentiate in an adult stem cell lineage.microPublication biology · 2025Article
- A developmental mechanism to regulate alternative polyadenylation in an adult stem cell lineage.Genes & development · 2024Article
- Integrating apaQTL and eQTL analysis identifies a potential causal variant associated with lung adenocarcinoma risk in the Chinese population.Communications biology · 2024Article
- A Developmental Mechanism to Regulate Alternative Polyadenylation in an Adult Stem Cell Lineage.bioRxiv : the preprint server for biology · 2024Article
- CSTF3 contributes to platinum resistance in ovarian cancer through alternative polyadenylation of lncRNA NEAT1 and generating the short isoform NEAT1_1.Cell death & disease · 2024Article
- Disruption of PABPN1 phase separation by SNRPD2 drives colorectal cancer cell proliferation and migration through promoting alternative polyadenylation of CTNNBIP1.Science China. Life sciences · 2024Article
- Alternative polyadenylation quantitative trait methylation mapping in human cancers provides clues into the molecular mechanisms of APA.American journal of human genetics · 2024Article
- CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone mRNA processing.RNA (New York, N.Y.) · 2024Article
- Nudt21-mediated alternative polyadenylation of MZT1 3'UTR contributes to pancreatic cancer progression.iScience · 2024Article
- Article
- Alternative polyadenylation landscape of longissimus dorsi muscle with high and low intramuscular fat content in cattle.Journal of animal science · 2024Article
- Alternative Polyadenylation Regulatory Factors Signature for Survival Prediction in Kidney Renal Cell Carcinoma.Cancer informatics · 2024Article
- Cell-type-specific alternative polyadenylation promotes oncogenic gene expression in non-small cell lung cancer progression.Molecular therapy. Nucleic acids · 2023Article
- NUDT21 alters glioma migration through differential alternative polyadenylation of LAMC1.Journal of neuro-oncology · 2023Article
- Transcriptomics-proteomics Integration reveals alternative polyadenylation driving inflammation-related protein translation in patients with diabetic nephropathy.Journal of translational medicine · 2023Article
- Relationship between NUDT21 mediated alternative polyadenylation process and tumor.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Alternative polyadenylation (APA) is a gene regulatory process that dictates mRNA 3'-UTR length, resulting in changes in mRNA stability and localization. APA is frequently disrupted in cancer and promotes tumorigenesis through altered expression of oncogenes and tumor suppressors. Pan-cancer analyses have revealed common APA events across the tumor landscape; however, little is known about tumor type-specific alterations that may uncover novel events and vulnerabilities. Here, we integrate RNA-sequencing data from the Genotype-Tissue Expression (GTEx) project and The Cancer Genome Atlas (TCGA) to comprehensively analyze APA events in 148 pancreatic ductal adenocarcinomas (PDACs). We report widespread, recurrent, and functionally relevant 3'-UTR alterations associated with gene expression changes of known and newly identified PDAC growth-promoting genes and experimentally validate the effects of these APA events on protein expression. We find enrichment for APA events in genes associated with known PDAC pathways, loss of tumor-suppressive miRNA binding sites, and increased heterogeneity in 3'-UTR forms of metabolic genes. Survival analyses reveal a subset of 3'-UTR alterations that independently characterize a poor prognostic cohort among PDAC patients. Finally, we identify and validate the casein kinase CSNK1A1 (also known as CK1alpha or CK1a) as an APA-regulated therapeutic target in PDAC. Knockdown or pharmacological inhibition of CSNK1A1 attenuates PDAC cell proliferation and clonogenic growth. Our single-cancer analysis reveals APA as an underappreciated driver of protumorigenic gene expression in PDAC via the loss of miRNA regulation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.