ArticleBlood2018
Epigenetic silencing of miR-125b is required for normal B-cell development.
Article in Blood, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 45 citations in OpenAlex.
- Review
- Overview of the Different Classes of Small RNAs During B-Cell Development.Methods in molecular biology (Clifton, N.J.) · 2025Review
- MiRNAs in Hematopoiesis and Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2023Review
- MicroRNA-125b as a valuable predictive marker for outcome after autologous hematopoietic stem cell transplantation.BMC cancer · 2023Article
- Review
- INK4 cyclin-dependent kinase inhibitors as potential prognostic biomarkers and therapeutic targets in hepatocellular carcinoma.Bioscience reports · 2022Article
- The emerging role non-coding RNAs in B cell-related disorders.Cancer cell international · 2022Review
- Competitive Endogenous RNA Network Involving miRNA and lncRNA in Non-Hodgkin Lymphoma: Current Advances and Clinical Perspectives.Biomedicines · 2021Review
- Article
- Potential of the tumor‑derived extracellular vesicles carrying the miR‑125b‑5p target TNFAIP3 in reducing the sensitivity of diffuse large B cell lymphoma to rituximab.International journal of oncology · 2021Observational
- The Multifaceted Role and Utility of MicroRNAs in Indolent B-Cell Non-Hodgkin Lymphomas.Biomedicines · 2021Review
- LncRNA UCA1 negatively regulates NF-kB activity in psoriatic keratinocytes through the miR125a-A20 axis.The Kaohsiung journal of medical sciences · 2021Article
- Article
- Review
- Essential functions of miR-125b in cancer.Cell proliferation · 2021Review
- Application of Hi-C and other omics data analysis in human cancer and cell differentiation research.Computational and structural biotechnology journal · 2021Review
- miRNA-Mediated Control of B Cell Responses in Immunity and SLE.Frontiers in immunology · 2021Review
- Review
- Acidic leucine-rich nuclear phosphoprotein-32A expression contributes to adverse outcome in acute myeloid leukemia.Annals of translational medicine · 2020Article
- The matrix vesicle cargo miR-125b accumulates in the bone matrix, inhibiting bone resorption in mice.Communications biology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Deregulation of several microRNAs (miRs) can influence critical developmental checkpoints during hematopoiesis as well as cell functions, eventually leading to the development of autoimmune disease or cancer. We found that miR-125b is expressed in bone marrow multipotent progenitors and myeloid cells but shut down in the B-cell lineage, and the gene encoding miR-125b lacked transcriptional activation markers in B cells. To understand the biological importance of the physiological silencing of miR-125b expression in B cells, we drove its expression in the B-cell lineage and found that dysregulated miR-125b expression impaired egress of immature B cells from the bone marrow to peripheral blood. Such impairment appeared to be mediated primarily by inhibited expression of the sphingosine-1-phosphate receptor 1 (S1PR1). Enforced expression of S1PR1 or clustered regularly interspaced short palindromic repeats/Cas9-mediated genome editing of the miR-125b targeting site in the S1PR1 3' untranslated region rescued the miR-125b-mediated defect in B-cell egress. In addition to impaired B-cell egress, miR-125b dysregulation initially reduced pre-B-cell output but later induced pre-B-cell lymphoma/leukemia in mice. Genetic deletion of IRF4 was found in miR-125b-induced B-cell cancer, but its role in oncogenic miR-125b-induced B-cell transformation is still unknown. Here, we further demonstrated an interaction of the effects of miR-125b and IRF4 in cancer induction by showing that miR125b-induced B-cell leukemia was greatly accelerated in IRF4 homozygous mutant mice. Thus, we conclude that physiological silencing of miR-125b is required for normal B-cell development and also acts as a mechanism of cancer suppression.
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Registered trials
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.