ArticleMolecular and cellular biology2011
QKI-mediated alternative splicing of the histone variant MacroH2A1 regulates cancer cell proliferation.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 149 citations in OpenAlex.
- Epithelial QKI Protects Against Emphysema by Maintaining Mitochondrial Integrity.bioRxiv : the preprint server for biology · 2026Article
- Histone variant H2A.J is an epigenetic regulator of metastasis in lung adenocarcinoma.Cell death & disease · 2026Article
- RNA-binding protein quaking: a multifunctional regulator in tumour progression.Annals of medicine · 2025Review
- Regional Conservation and Transcriptional Regulation of Tumor-Associated Genes by macroH2A1 Deposition in Mammalian Cells.Biomolecules · 2025Article
- Genetic variants of LncRNA associated with splicing regulation and their impact on ovarian cancer development.Functional & integrative genomics · 2025Article
- Epigenetic control of topoisomerase 1 activity presents a cancer vulnerability.Nature communications · 2025Article
- BiFC and FACS-based CRISPR screening revealed that QKI promotes PABPN1 LLPS in colorectal cancer cells.Protein & cell · 2025Article
- Histone variants: key regulators of inflammation in cell dedifferentiation and transdifferentiation.Frontiers in immunology · 2025Review
- The crosstalk between alternative splicing and circular RNA in cancer: pathogenic insights and therapeutic implications.Cellular & molecular biology letters · 2024Review
- Mature microRNA-binding protein QKI suppresses extracellular microRNA let-7b release.Journal of cell science · 2024Article
- The Function of H2A Histone Variants and Their Roles in Diseases.Biomolecules · 2024Review
- GAS5 regulated by FTO-mediated m6A modification suppresses cell proliferation via the IGF2BP2/QKI axis in breast cancer.Discover oncology · 2024Article
- Exploring the interplay between PARP1 and circRNA biogenesis and function.Wiley interdisciplinary reviews. RNA · 2023Review
- macroH2A2 antagonizes epigenetic programs of stemness in glioblastoma.Nature communications · 2023Article
- MacroH2A histone variants modulate enhancer activity to repress oncogenic programs and cellular reprogramming.Communications biology · 2023Article
- RNA-Binding Proteins in Bladder Cancer.Cancers · 2023Review
- Targeted splicing therapy: new strategies for colorectal cancer.Frontiers in oncology · 2023Review
- The histone variant macroH2A1.1 regulates RNA polymerase II-paused genes within defined chromatin interaction landscapes.Journal of cell science · 2022Article
- Histone Variant macroH2A1.1 Enhances Nonhomologous End Joining-dependent DNA Double-strand-break Repair and Reprogramming Efficiency of Human iPSCs.Stem cells (Dayton, Ohio) · 2022Article
- Unconventional metabolites in chromatin regulation.Bioscience reports · 2022Article
48 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histone variant macroH2A1 contains a carboxyl-terminal ∼30-kDa domain called a macro domain. MacroH2A1 is produced as one of two alternatively spliced forms, macroH2A1.1 and macroH2A1.2. While the macro domain of macroH2A1.1 can interact with NAD(+)-derived small molecules, such as poly(ADP-ribose), macroH2A1.2's macro domain cannot. Here, we show that changes in the alternative splicing of macroH2A1 pre-mRNA, which lead to a decrease in macroH2A1.1 expression, occur in a variety of cancers, including testicular, lung, bladder, cervical, breast, colon, ovarian, and endometrial. Furthermore, reintroduction of macroH2A1.1 suppresses the proliferation of lung and cervical cancer cells in a manner that requires the ability of macroH2A1.1 to bind NAD(+)-derived metabolites. MacroH2A1.1-mediated suppression of proliferation occurs, at least in part, through the reduction of poly(ADP-ribose) polymerase 1 (PARP-1) protein levels. By analyzing publically available expression and splicing microarray data, we identified splicing factors that correlate with alterations in macroH2A1 splicing. Using RNA interference, we demonstrate that one of these factors, QKI, regulates the alternative splicing of macroH2A1 pre-mRNA, resulting in increased levels of macroH2A1.1. Finally, we demonstrate that QKI expression is significantly reduced in many of the same cancer types that demonstrate a reduction in macroH2A1.1 splicing.
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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.