ArticleScientific reports2018
Histone Variant MacroH2A1 Plays an Isoform-Specific Role in Suppressing Epithelial-Mesenchymal Transition.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Multifunctional histone variants in genome function.Nature reviews. Genetics · 2025Review
- Identification of a novel DNA oxidative damage repair pathway, requiring the ubiquitination of the histone variant macroH2A1.1.BMC biology · 2024Article
- The Function of H2A Histone Variants and Their Roles in Diseases.Biomolecules · 2024Review
- Roles of Histone H2A Variants in Cancer Development, Prognosis, and Treatment.International journal of molecular sciences · 2024Review
- PRNP is a pan-cancer prognostic and immunity-related to EMT in colorectal cancer.Frontiers in cell and developmental biology · 2024Article
- The epithelial-mesenchymal plasticity landscape: principles of design and mechanisms of regulation.Nature reviews. Genetics · 2023Review
- MacroH2A histone variants modulate enhancer activity to repress oncogenic programs and cellular reprogramming.Communications biology · 2023Article
- Combinatorial targeting of a specific EMT/MET network by macroH2A variants safeguards mesenchymal identity.PloS one · 2023Article
- Ten Years of CRISPRing Cancers In Vitro.Cancers · 2022Review
- Article
- MALDI-MSI: A Powerful Approach to Understand Primary Pancreatic Ductal Adenocarcinoma and Metastases.Molecules (Basel, Switzerland) · 2022Article
- Joining the PARty: PARP Regulation of KDM5A during DNA Repair (and Transcription?).BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Review
- 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
- The Invasion and Metastasis of Colon Adenocarcinoma (COAD) Induced by SALL4.Journal of immunology research · 2022Article
- MacroH2A1.1 has evolved to let PARP1 do more by loosening its grip on PAR.Nature structural & molecular biology · 2021Article
- Mutant U2AF1-induced alternative splicing of H2afy (macroH2A1) regulates B-lymphopoiesis in mice.Cell reports · 2021Article
- The Role of MacroH2A Histone Variants in Cancer.Cancers · 2021Review
- Article
- Solid tumours hijack the histone variant network.Nature reviews. Cancer · 2021Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Epithelial-Mesenchymal Transition (EMT) is a biological program that plays key roles in various developmental and pathological processes. Although much work has been done on signaling pathways and transcription factors regulating EMT, the epigenetic regulation of EMT remains not well understood. Histone variants have been recognized as a key group of epigenetic regulators. Among them, macroH2A1 is involved in stem cell reprogramming and cancer progression. We postulated that macroH2A1 may play a role in EMT, a process involving reprogramming of cellular states. In this study, we demonstrate that expression of macroH2A1 is dramatically reduced during EMT induction in immortalized human mammary epithelial cells (HMLE). Moreover, ectopic expression of the macroH2A1.1 isoform, but not macroH2A1.2, can suppress EMT induction and reduce the stem-like cell population in HMLE. Interestingly, macroH2A1.1 overexpression cannot revert stable mesenchymal cells back to the epithelial state, suggesting a stage-specific role of macroH2A1.1 in EMT. We further pinpointed that the function of macroH2A1.1 in EMT suppression is dependent on its ability to bind the NAD
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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.