ArticlePloS one2012
TSA suppresses miR-106b-93-25 cluster expression through downregulation of MYC and inhibits proliferation and induces apoptosis in human EMC.
Article in PloS one, 2012. 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, 53 citations in OpenAlex.
- Circulating microRNAs as diagnostic biomarkers and pathogenic mediators in type 2 diabetic retinopathy: a systematic review.Acta diabetologica · 2026Review
- Building a Hand-Curated ceRNET for Endometrial Cancer, Striving for Clinical as Well as Medicolegal Soundness: A Systematic Review.Non-coding RNA · 2025Review
- Overview of miR-106a Regulatory Roles: from Cancer to Aging.Bioengineering (Basel, Switzerland) · 2023Review
- Epigenetic therapy reprograms M2-type tumor-associated macrophages into an M1-like phenotype by upregulating miR-7083-5p.Frontiers in immunology · 2022Article
- Circular RNA Circ_0000677 promotes cell proliferation by regulating microRNA-106b-5p/CCND1 in non-small cell lung cancer.Bioengineered · 2021Article
- Integrated pan-cancer of AURKA expression and drug sensitivity analysis reveals increased expression of AURKA is responsible for drug resistance.Cancer medicine · 2021Article
- Epigenetic Deregulation of Apoptosis in Cancers.Cancers · 2021Review
- Non-Coding RNAs as Prognostic Markers for Endometrial Cancer.International journal of molecular sciences · 2021Review
- Review
- Oxidative stress-induced mitophagy is suppressed by the miR-106b-93-25 cluster in a protective manner.Cell death & disease · 2021Article
- Histone Deacetylase Inhibitors: A Promising Therapeutic Alternative for Endometrial Carcinoma.Disease markers · 2021Review
- Integrative p53, micro-RNA and Cathepsin Protease Co-Regulatory Expression Networks in Cancer.Cancers · 2020Review
- Histone Deacetylase Modifications by Probiotics in Colorectal Cancer.Journal of gastrointestinal cancer · 2020Review
- IL-6 promotes PD-L1 expression in monocytes and macrophages by decreasing protein tyrosine phosphatase receptor type O expression in human hepatocellular carcinoma.Journal for immunotherapy of cancer · 2020Article
- Expression of serum Hsa-miR-93 in uterine cancer and its clinical significance.Oncology letters · 2018Article
- Grape seed procyanidin extract against lung cancer: the role of microrna-106b, bioavailability, and bioactivity.Oncotarget · 2018Article
- NRF2 regulates endothelial glycolysis and proliferation with miR-93 and mediates the effects of oxidized phospholipids on endothelial activation.Nucleic acids research · 2018Article
- Article
- An Antagomir to MicroRNA-106b-5p Ameliorates Cerebral Ischemia and Reperfusion Injury in Rats Via Inhibiting Apoptosis and Oxidative Stress.Molecular neurobiology · 2017Article
- Integrative analysis of signaling pathways and diseases associated with the miR-106b/25 cluster and their function study in berberine-induced multiple myeloma cells.Functional & integrative genomics · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase (HDAC) inhibitors are emerging as a novel class of anti-tumor agents and have manifested the ability to decrease proliferation and increase apoptosis in different cancer cells. A significant number of genes have been identified as potential effectors responsible for the anti-tumor function of HDAC inhibitor. However, the molecular mechanisms of these HDAC inhibitors in this process remain largely undefined. In the current study, we searched for microRNAs (miRs) that were affected by HDAC inhibitor trichostatin (TSA) and investigated their effects in endometrial cancer (EMC) cells. Our data showed that TSA significantly inhibited the growth of EMC cells and induced their apoptosis. Among the miRNAs that altered in the presence of TSA, the miR-106b-93-25 cluster, together with its host gene MCM7, were obviously down-regulated in EMC cells. p21 and BIM, which were identified as target genes of miR-106b-93-25 cluster, increased in TSA treated tumor cells and were responsible for cell cycle arrest and apoptosis. We further identified MYC as a regulator of miR-106b-93-25 cluster and demonstrated its down-regulation in the presence of TSA resulted in the reduction of miR-106b-93-25 cluster and up-regulation of p21 and BIM. More important, we found miR-106b-93-25 cluster was up-regulated in clinical EMC samples in association with the overexpression of MCM7 and MYC and the down-regulation of p21 and BIM. Thus our studies strongly indicated TSA inhibited EMC cell growth and induced cell apoptosis and cell cycle arrest at least partially through the down-regulation of the miR-106b-93-25 cluster and up-regulation of it's target genes p21 and BIM via MYC.
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