ArticleBlood2012
Histone deacetylases mediate the silencing of miR-15a, miR-16, and miR-29b in chronic lymphocytic leukemia.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
108 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.
- Association of the Expression Level of miR-16 with Prognosis of Solid Cancer Patients: A Meta-Analysis and Bioinformatic Analysis.Disease markers · 2020Pooled it
- The Life of MicroRNAs: Biogenesis, Function and Decay in Cancer.Biomolecules · 2025Review
- MircoRNAs predict and modulate responses to chemotherapy in leukemic patients.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The Role of MicroRNAs, CircRNAs, and LncRNAs in Chronic Lymphocytic Leukemia.Current pharmaceutical design · 2025Review
- Role of exosome-derived miRNAs in diabetic wound angiogenesis.Molecular and cellular biochemistry · 2024Review
- Immune escape of multiple myeloma cells results from low miR29b and the ensuing epigenetic silencing of proteasome genes.Biomarker research · 2024Article
- CMC: Cancer miRNA Census - a list of cancer-related miRNA genes.Nucleic acids research · 2024Article
- MicroRNAs: Potential prognostic and theranostic biomarkers in chronic lymphocytic leukemia.EJHaem · 2024Review
- MicroRNA-Mediated Regulation of Histone-Modifying Enzymes in Cancer: Mechanisms and Therapeutic Implications.Biomolecules · 2023Review
- Role of microRNAs in Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2023Review
- HDAC1 regulates the chromatin landscape to control transcriptional dependencies in chronic lymphocytic leukemia.Blood advances · 2023Article
- Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Abnormal regulation of miR-29b-ID1 signaling is involved in the process of decitabine resistance in leukemia cells.Cell cycle (Georgetown, Tex.) · 2023Article
- Chromatin and Cancer: Implications of Disrupted Chromatin Organization in Tumorigenesis and Its Diversification.Cancers · 2023Review
- Apoptosis evasion via long non-coding RNAs in colorectal cancer.Cancer cell international · 2022Review
- The paradigm of drug resistance in cancer: an epigenetic perspective.Bioscience reports · 2022Review
- Nucleic Acid Biomarkers in Waldenström Macroglobulinemia and IgM-MGUS: Current Insights and Clinical Relevance.Diagnostics (Basel, Switzerland) · 2022Review
- A Boolean Model of the Proliferative Role of the lncRNA XIST in Non-Small Cell Lung Cancer Cells.Biology · 2022Article
- The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role.Molecular cancer · 2022Review
- Consequences of genetic variants in miRNA genes.Computational and structural biotechnology journal · 2022Review
48 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Chronic lymphocytic leukemia (CLL) demonstrates a global down-regulation of miR-15a and miR-16 and a selective silencing of the related miR-29b in aggressive disease. Deletions in chromosome 13 [del(13q14)] partially account for the loss of expression of miR-15a and miR-16, but the mechanisms by which miR-29b becomes silenced is unknown. In the present study, we show that the histone deacetylases (HDACs) are overexpressed in CLL and mediate the epigenetic silencing of miR-15a, miR-16, and miR-29b. HDAC inhibition triggered the accumulation of the transcriptionally activating chromatin modification H3K4me2 and restored the expression of miR-15a, miR-16, and miR-29b in approximately 35% of samples. Ectopic expression of miR-15a and miR-16 and HDAC inhibition-induced expression of miR-15a, miR-16, or miR-29b in primary CLL cells was associated with declines in the levels of Mcl-1, but not Bcl-2, mitochondrial dysfunction, and induction of cell death. Therefore, our results show that HDACs aberrantly silence the expression of the critical tumor suppressors miR-15a, miR-16, and miR-29b in CLL. Deacetylase inhibition may be a therapeutic strategy that restores the expression of these miRs to antagonize Mcl-1, an important survival protein in these cells. Consequently, CLL patients who exhibit such epigenetic silencing may benefit from HDAC inhibitor-based therapy.
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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.