ArticlePLoS genetics2017
The co-existence of transcriptional activator and transcriptional repressor MEF2 complexes influences tumor aggressiveness.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- MEF2C induces intrinsic apoptosis and reverses cisplatin resistance in A2780 ovarian cancer cell line.BMC cancer · 2025Article
- Identification of a novel minor-groove DNA binder that represses mitochondrial gene expression and induces apoptosis in highly aggressive leiomyosarcoma cells.Cell death discovery · 2025Article
- Alternative Promoters Drive Transcriptomic Reprogramming and Prognostic Stratification in TNBC.NPJ systems biology and applications · 2025Article
- HDAC9 Deficiency Upregulates cGMP-dependent Kinase II to Mitigate Neuronal Apoptosis in Ischemic Stroke.Translational stroke research · 2025Article
- A Comprehensive Bioinformatic Analysis Based on Functional Studies of MEF-2 Family in NSCLC.The Yale journal of biology and medicine · 2025Article
- Article
- MEF2D Functions as a Tumor Suppressor in Breast Cancer.International journal of molecular sciences · 2024Article
- TheThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Targeting histone deacetylase 9 represses fibrogenic phenotypes in buccal mucosal fibroblasts with arecoline stimulation.Journal of dental sciences · 2024Article
- The Molecular and Biological Function of MEF2D in Leukemia.Advances in experimental medicine and biology · 2024Review
- Inference of differential gene regulatory networks using boosted differential trees.Bioinformatics advances · 2024Article
- Bioactive Compounds and Cardiac Fibrosis: Current Insight and Future Prospect.Journal of cardiovascular development and disease · 2023Review
- Myocyte Enhancer Factor 2A Plays a Central Role in the Regulatory Networks of Cellular Physiopathology.Aging and disease · 2023Review
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
- Regulation of human T-cell leukemia virus type 1 antisense promoter by myocyte enhancer factor-2C in the context of adult T-cell leukemia and lymphoma.Haematologica · 2022Article
- Transcriptomic and genomic studies classify NKL54 as a histone deacetylase inhibitor with indirect influence on MEF2-dependent transcription.Nucleic acids research · 2022Article
- Clusterin suppresses invasion and metastasis of testicular seminoma by upregulating COL15a1.Molecular therapy. Nucleic acids · 2021Article
- The Wnt pathway: An important control mechanism in bone's response to mechanical loading.Bone · 2021Review
- Histone deacetylase (HDAC) 9: versatile biological functions and emerging roles in human cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- HDAC4 degradation during senescence unleashes an epigenetic program driven by AP-1/p300 at selected enhancers and super-enhancers.Genome biology · 2021Article
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11 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The contribution of MEF2 TFs to the tumorigenic process is still mysterious. Here we clarify that MEF2 can support both pro-oncogenic or tumor suppressive activities depending on the interaction with co-activators or co-repressors partners. Through these interactions MEF2 supervise histone modifications associated with gene activation/repression, such as H3K4 methylation and H3K27 acetylation. Critical switches for the generation of a MEF2 repressive environment are class IIa HDACs. In leiomyosarcomas (LMS), this two-faced trait of MEF2 is relevant for tumor aggressiveness. Class IIa HDACs are overexpressed in 22% of LMS, where high levels of MEF2, HDAC4 and HDAC9 inversely correlate with overall survival. The knock out of HDAC9 suppresses the transformed phenotype of LMS cells, by restoring the transcriptional proficiency of some MEF2-target loci. HDAC9 coordinates also the demethylation of H3K4me3 at the promoters of MEF2-target genes. Moreover, we show that class IIa HDACs do not bind all the regulative elements bound by MEF2. Hence, in a cell MEF2-target genes actively transcribed and strongly repressed can coexist. However, these repressed MEF2-targets are poised in terms of chromatin signature. Overall our results candidate class IIa HDACs and HDAC9 in particular, as druggable targets for a therapeutic intervention in LMS.
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