ArticleOncogene2018
Activating and sustaining c-Myc by depletion of miR-144/451 gene locus contributes to B-lymphomagenesis.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- miR-144/451: A Regulatory Role in Inflammation.Current molecular medicine · 2025Review
- c-Myc inhibits LAPTM5 expression in B-cell lymphomas.Annals of hematology · 2023Article
- Crosstalk betweenGenes · 2023Article
- Epigenetic modulations of immune cells: from normal development to tumor progression.International journal of biological sciences · 2023Review
- p63, a key regulator of Ago2, links to the microRNA-144 cluster.Cell death & disease · 2022Article
- β-catenin links cell seeding density to global gene expression during mouse embryonic stem cell differentiation.iScience · 2022Article
- microRNA-144/451 decreases dendritic cell bioactivityFrontiers in immunology · 2022Article
- PMMS: Predicting essential miRNAs based on multi-head self-attention mechanism and sequences.Frontiers in medicine · 2022Article
- miRNA- and lncRNA-Based Therapeutics for Non-Hodgkin's Lymphoma: Moving towards an RNA-Guided Precision Medicine.Cancers · 2021Review
- Insights about MYC and Apoptosis in B-Lymphomagenesis: An Update from Murine Models.International journal of molecular sciences · 2020Review
- miR-144-5p and miR-451a Inhibit the Growth of Cholangiocarcinoma Cells Through Decreasing the Expression of ST8SIA4.Frontiers in oncology · 2020Article
- The Role of Noncoding RNAs in B-Cell Lymphoma.Frontiers in oncology · 2020Review
- Intricate crosstalk between MYC and non-coding RNAs regulates hallmarks of cancer.Molecular oncology · 2019Review
- Metazoan MicroRNAs.Cell · 2018Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyper activity of protooncogene c-Myc is one of the hallmarks of highly aggressive lymphomas. However, the mechanism of how c-Myc is subjected to activation and amplification is still not well defined. In this study, we use gene knockout strategy to show that targeted depletion of a well-conserved microRNA gene locus miR-144/451 initiates tumorigenesis including B-lymphoma development in aged mice. This is due, at least in part, to the direct activation of the c-Myc gene by loss of miR-144/451 expression in hematopoietic cells. Moreover, oncoprotein c-Myc inversely regulates miR-144/451 expression by directly binding to the miR-144/451 promoter region, forming a miRNA-Myc positive feedback loop to safeguard the high level of c-Myc in B-lymphocytes. We also demonstrate that this miRNA-Myc crosstalk is disrupted in human diffuse large B-cell lymphomas with aberrant c-Myc expression. Therefore, our findings provide strong evidence, for the first time, that deficiency of miR-144/451 expression may play a bona fide role in derepression of silenced c-Myc, which contributes to tumor development including B-lymphomagenesis.
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Registered trials
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