ArticleGenes & development2014
An integrative analysis of colon cancer identifies an essential function for PRPF6 in tumor growth.
Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Pooled it
- Mechanism-based prediction of drug synergy via network controllability analysis of therapeutic pathways in intractable diseases.iScience · 2026Article
- Profiling gut microbiota of colorectal cancer in Indonesia: a focus on beneficial taxa depletion.Gut pathogens · 2026Article
- ZAK kinase at the crossroads of cellular stress: functional plasticity, human pathobiology, and precision therapeutics.Frontiers in cell and developmental biology · 2026Review
- USP13 Facilitates the Proliferation of Hepatocellular Carcinoma Cells by Reducing K48/63-Linked Polyubiquitination and Degradation of PRPF6.Journal of cellular and molecular medicine · 2025Article
- Dysregulated ribosome quality control in human diseases.The FEBS journal · 2025Review
- PAIP1 binds to pre-mRNA and regulates alternative splicing of cancer pathway genes including VEGFA.BMC genomics · 2024Article
- Spliceosomic dysregulation in pancreatic cancer uncovers splicing factors PRPF8 and RBMX as novel candidate actionable targets.Molecular oncology · 2024Article
- Identification of novel molecular subtypes to improve the classification framework of nasopharyngeal carcinoma.British journal of cancer · 2024Article
- Xrp1 governs the stress response program to spliceosome dysfunction.Nucleic acids research · 2024Article
- Article
- Alternative mRNA Splicing and Promising Therapies in Cancer.Biomolecules · 2023Review
- Article
- Data mining identifies novel RNA-binding proteins involved in colon and rectal carcinomas.Frontiers in cell and developmental biology · 2023Article
- Article
- Aberrant Retinal Pigment Epithelial Cells Derived from Induced Pluripotent Stem Cells of a Retinitis Pigmentosa Patient with the PRPF6 Mutation.International journal of molecular sciences · 2022Article
- Emerging roles of spliceosome in cancer and immunity.Protein & cell · 2022Review
- Hereditary retinoblastoma iPSC model reveals aberrant spliceosome function driving bone malignancies.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Alternative splicing of mRNA in colorectal cancer: new strategies for tumor diagnosis and treatment.Cell death & disease · 2021Review
- CD44 alternative splicing senses intragenic DNA methylation in tumors via direct and indirect mechanisms.Nucleic acids research · 2021Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
22 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spliceosome machinery is composed of multimeric protein complexes that generate a diverse repertoire of mRNA through coordinated splicing of heteronuclear RNAs. While somatic mutations in spliceosome components have been discovered in several cancer types, the molecular bases and consequences of spliceosome aberrations in cancer are poorly understood. Here we report for the first time that PRPF6, a member of the tri-snRNP (small ribonucleoprotein) spliceosome complex, drives cancer proliferation by preferential splicing of genes associated with growth regulation. Inhibition of PRPF6 and other tri-snRNP complex proteins, but not other snRNP spliceosome complexes, selectively abrogated growth in cancer cells with high tri-snRNP levels. High-resolution transcriptome analyses revealed that reduced PRPF6 alters the constitutive and alternative splicing of a discrete number of genes, including an oncogenic isoform of the ZAK kinase. These findings implicate an essential role for PRPF6 in cancer via splicing of distinct growth-related gene products.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.