ArticleJournal of cancer research and clinical oncology2018
MiR-29 silencing modulates the expression of target genes related to proliferation, apoptosis and methylation in Burkitt lymphoma cells.
Article in Journal of cancer research and clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Repression of miR-29 via MYC leads to increased CD40 signaling in transformed follicular lymphoma.Leukemia · 2026Trial
- Mutual feedback regulation between Poly(A)-specific ribonuclease (PARN) and cognate microRNAs.Life science alliance · 2026Article
- MiRNAs as new potential biomarkers and therapeutic targets in brain metastasis.Non-coding RNA research · 2024Review
- Immune escape of multiple myeloma cells results from low miR29b and the ensuing epigenetic silencing of proteasome genes.Biomarker research · 2024Article
- DNA Methyltransferases: From Evolution to Clinical Applications.International journal of molecular sciences · 2022Review
- Review
- Epigenetic regulation of miR-518a-5p-CCR6 feedback loop promotes both proliferation and invasion in diffuse large B cell lymphoma.Epigenetics · 2021Article
- Epigenetic Regulation of miR-92a and TET2 and Their Association in Non-Hodgkin Lymphoma.Frontiers in genetics · 2021Article
- Combination of Decitabine and a Modified Regimen of Cisplatin, Cytarabine and Dexamethasone: A Potential Salvage Regimen for Relapsed or Refractory Diffuse Large B-Cell Lymphoma After Second-Line Treatment Failure.Frontiers in oncology · 2021Article
- Article
- When Oxidative Stress Meets Epigenetics: Implications in Cancer Development.Antioxidants (Basel, Switzerland) · 2020Review
- Hypoxia-induced apoptosis of cardiomyocytes is restricted by ginkgolide B-downregulated microRNA-29.Cell cycle (Georgetown, Tex.) · 2020Article
- miR-29a Is Repressed by MYC in Pancreatic Cancer and Its Restoration Drives Tumor-Suppressive Effects via Downregulation of LOXL2.Molecular cancer research : MCR · 2020Article
- MicroRNA-29 family inhibits rhabdomyosarcoma formation and progression by regulating GEFT function.American journal of translational research · 2020Article
- Molecular biomarkers in diabetes mellitus (DM).Medical journal of the Islamic Republic of Iran · 2020Review
- Major miRNA Involved in Insulin Secretion and Production in Beta-Cells.International journal of general medicine · 2020Review
- The Role of Noncoding RNAs in B-Cell Lymphoma.Frontiers in oncology · 2020Review
- Germinal Centre B Cell Functions and Lymphomagenesis: Circuits Involving MYC and MicroRNAs.Cells · 2019Review
- MicroRNA Networks Modulate Oxidative Stress in Cancer.International journal of molecular sciences · 2019Review
- Restoration of microRNA-29c in type I endometrioid cancer reduced endometrial cancer cell growth.Oncology letters · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
purposeBurkitt lymphoma (BL) is a B-cell lymphoma frequently diagnosed in children. It is characterized by MYC translocations, which lead to the constitutive expression of the MYC oncogene. MYC contributes to miR-29 repression through an E-box MYC binding site on the miR-29b-1/miR-29a promoter region. We evaluated the role of miR-29a/b/c and their predicted targets in BL pathogenesis.
methodsMature sequences of miR-29a/b/c were transfected to the BL cell lines BL41 and Raji, and evaluated for DNMT3B, MCL1, BIM, CDK6, AKT and TCL1 protein expression as well as for MCL-1 and CDK6 mRNA expression. BL cells were treated with 5-aza-2'-deoxycytidine (decitabine) and evaluated for miR29 expressions and methylation status. DNMT3B inhibition was performed by DNMT3B siRNA.
resultsEctopic expression of miR-29s in BL cells decreased CDK6, DNMT3B, TCL1 and MCL-1 protein levels, but CDK6 and MCL-1 mRNA expression was unaffected by miR-29. Decitabine enhanced miR-29 expression levels and decreased CDK6 protein expression. Additionally, inhibition of DNMT3B by siRNA increased miR-29a/b expression. Notably, the miR-29a/b1 and miR-29b2/c promoter genes showed methylated CpG sequences that were demethylated after decitabine treatments. Furthermore, MYC-negative tumours had higher levels of miR-29 expression compared with MYC-translocated cases, suggesting that MYC regulates miR-29 in BL tumours.
conclusionsOur results suggest a significant role for miR-29s in BL pathogenesis in altering the expression of targets involved in critical cancer pathways, such as cell cycle control, apoptosis inhibition and DNA methylation. Moreover, methylation-mediated miR-29 epigenetic silencing may occur during BL development.
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