ArticleAmerican journal of translational research2016
miR-125b regulates cell progression in chronic myeloid leukemia via targeting BAK1.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Investigating autophagy and miRNAs as therapeutic targets in leukemia.Discover oncology · 2026Review
- Single-cell disentangled representations for perturbation modeling and treatment effect estimation.bioRxiv : the preprint server for biology · 2026Article
- Danhong Injection Up-regulates miR-125b in Endothelial Exosomes and Attenuates Apoptosis in Post-Infarction Myocardium.Chinese journal of integrative medicine · 2023Article
- Tumour‑derived exosomes and their emerging roles in leukaemia (Review).Experimental and therapeutic medicine · 2023Review
- CD33-targeting extracellular vesicles deliver antisense oligonucleotides against FLT3-ITD and miR-125b for specific treatment of acute myeloid leukaemia.Cell proliferation · 2022Article
- Multi-ancestry fine-mapping improves precision to identify causal genes in transcriptome-wide association studies.American journal of human genetics · 2022Article
- Hcmv-miR-UL148D regulates the staurosporine-induced apoptosis by targeting the Endoplasmic Reticulum to Nucleus signaling 1(ERN1).PloS one · 2022Article
- Essential functions of miR-125b in cancer.Cell proliferation · 2021Review
- MiR-125b promotes migration and invasion by targeting the vitamin D receptor in renal cell carcinoma.International journal of medical sciences · 2021Observational
- Downregulation of miR-142a Contributes to the Enhanced Anti-Apoptotic Ability of Murine Chronic Myelogenous Leukemia Cells.Frontiers in oncology · 2021Article
- miR-125b Upregulates miR-34a and Sequentially Activates Stress Adaption and Cell Death Mechanisms in Multiple Myeloma.Molecular therapy. Nucleic acids · 2019Article
- miR-125b-5p and miR-99a-5p downregulate human γδ T-cell activation and cytotoxicity.Cellular & molecular immunology · 2019Article
- A carvedilol-responsive microRNA, miR-125b-5p protects the heart from acute myocardial infarction by repressing pro-apoptotic bak1 and klf13 in cardiomyocytes.Journal of molecular and cellular cardiology · 2018Article
- Hypoxia-elicited mesenchymal stem cell-derived exosomes facilitates cardiac repair through miR-125b-mediated prevention of cell death in myocardial infarction.Theranostics · 2018Article
- Downregulation of microRNA-125a is involved in intervertebral disc degeneration by targeting pro-apoptotic Bcl-2 antagonist killer 1.Iranian journal of basic medical sciences · 2017Article
- The trophoblast cell surface antigen 2 and miR-125b axis in urothelial bladder cancer.Oncotarget · 2017Article
- Exosomes derived from human umbilical cord mesenchymal stem cells protect against cisplatin-induced ovarian granulosa cell stress and apoptosis in vitro.Scientific reports · 2017Article
- microRNAs and Acute Myeloid Leukemia Chemoresistance: A Mechanistic Overview.Frontiers in oncology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a type of malignant tumor characterized by the accumulation of a large number of immature white blood cells in the blood and bone marrow. BAK1 was predicted to be the target gene of microRNA-451 (miR-125b). The present study was designed to illustrate the mechanism of miR-125b in regulating CML via targeting BAK1. In this study, we found that the expression of miR-125b increased strongly, whereas the expression of BAK1 decreased significantly in CML patients and CML cell lines compared with healthy controls. Moreover, the luciferase report assay confirmed the interaction between miR-125b and BAK1 mRNA. After transfection of the miR-125b mimic or miR-125b inhibitor into CML cells, we found that the inhibition of miR-125b decreased the proliferation rates and promoted apoptosis with cell cycle arrest at the G0/G1 phase in both K562 and NB-4 cells, increased the expression of BAK1 and Caspase-3, and decreased the expression of Bcl-2 and c-myc; the miR-125b mimic yielded the opposite results. In addition, siBAK1 offset the suppression effect of the miR-125b inhibitor in K562 cells, indicating that miR-125b promotes these cellular processes by inhibiting the expression of BAK1. Further in vivo experiments supported these findings because miR-125b suppression reduced CML growth in mice. Taken together, our study suggests that the down-regulation of miR-125b affects the expression of BAK1, promotes cell apoptosis and inhibits cell proliferation, leading to up-regulated expression of pro-apoptosis factors, down-regulated expression of anti-apoptosis factors in the mitochondrial apoptotic pathway, and decreased tumor size and weight of CML in vivo. These results provide a potential therapeutic strategy for CML.
Indexed as
Identifiers
27158338PMC4846895W2396612800What OpenQuestion holds
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.