ArticleOncogene2014
BCR-ABL/GATA1/miR-138 mini circuitry contributes to the leukemogenesis of chronic myeloid leukemia.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 83 citations in OpenAlex.
- Transient High-Glucose Exposure and Erk Signaling.Circulation reports · 2026Article
- Impact of non-coding RNAs on resistance to imatinib in chronic myelogenous leukemia.Leukemia research reports · 2025Review
- Role of miRNAs to control the progression of Chronic Myeloid Leukemia by their expression levels.Medical oncology (Northwood, London, England) · 2024Review
- Enabling biomedical technologies for chronic myelogenous leukemia (CML) biomarkers detection.Biomicrofluidics · 2024Review
- Establishment of the Myeloid TBX-Code Reveals Aberrant Expression of T-Box Gene TBX1 in Chronic Myeloid Leukemia.International journal of molecular sciences · 2023Article
- Insight into microRNAs' involvement in hematopoiesis: current standing point of findings.Stem cell research & therapy · 2023Review
- NDRG3 regulates imatinib resistance by promoting β‑catenin accumulation in the nucleus in chronic myelogenous leukemia.Oncology reports · 2023Article
- Over-Expressed GATA-1Antioxidants (Basel, Switzerland) · 2023Article
- MicroRNA-138-5p Targets Pro-Apoptotic Factors and Favors Neural Cell Survival: Analysis in the Injured Spinal Cord.Biomedicines · 2022Article
- Non-coding RNAs: are they the protagonist or antagonist in the regulation of leukemia?American journal of translational research · 2022Review
- Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?International journal of molecular sciences · 2021Review
- Exploring the Leukemogenic Potential of GATA-1Antioxidants (Basel, Switzerland) · 2021Article
- Circular RNA SAMD4A controls adipogenesis in obesity through the miR-138-5p/EZH2 axis.Theranostics · 2020Article
- Non-coding RNAs in cancers with chromosomal rearrangements: the signatures, causes, functions and implications.Journal of molecular cell biology · 2019Review
- Hyaluronan abrogates imatinib-induced senescence in chronic myeloid leukemia cell lines.Scientific reports · 2019Article
- Pivotal role of microRNA-138 in human cancers.American journal of cancer research · 2019Review
- Overexpression of miR-4433 by suberoylanilide hydroxamic acid suppresses growth of CML cells and induces apoptosis through targeting Bcr-Abl.Journal of Cancer · 2019Article
- [MicroRNA-138 regulates cell adhesion-mediated drug resistance phenotype by targeting SGTA in non-Hodgkin's lymphoma].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2018Article
- Egr2-dependent microRNA-138 is dispensable for peripheral nerve myelination.Scientific reports · 2018Article
- The Network of Non-coding RNAs in Cancer Drug Resistance.Frontiers in oncology · 2018Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal expression of microRNAs (miRNAs) has been implicated in carcinogenesis. Here we report a novel BCR (breakpoint cluster region)-ABL (c-abl oncogene 1, non-receptor tyrosine kinase)/GATA1/microRNA-138 (miR-138) circuitry in chronic myeloid leukemia (CML). miR-138 expression is downregulated in K562 cells and primary CML samples, which is restored after imatinib treatment. The tumor suppressor activity of miR-138 is demonstrated by the induction of cell cycle arrest at G0/G1, inhibition of cell proliferation and colony forming unit granulocyte-macrophage colony formation and enhanced imatinib-induced apoptosis in K562 and Ku812 cells overexpressing miR-138. Moreover, overexpression of miR-138 led to the downregulation of BCR-ABL. Based on luciferase assay, ABL and BCR-ABL are shown to be the target genes regulated by miR-138. Furthermore, miR-138 binding to ABL was shown to localize to the coding region instead of 3'-untranslated regions (3'-UTR) of ABL mRNA. In addition, CCND3 is another target of miR-138, which represses CCND3 expression by binding to its 3'-UTR. Finally, upregulation of miR-138 upon imatinib treatment is associated with the enhancement of GATA1 activity, which binds to the miR-138 promoter. In conclusion, miR-138 is a tumor suppressor miRNA underexpressed in CML. miR-138 represses expression of both BCR-ABL and CCND3 via binding to the coding region and 3'-UTR, respectively. miR-138 expression is activated by GATA1, which in turn is repressed by BCR-ABL. Therefore, miR-138, by virtue of a BCR-ABL/GATA1/miR-138 circuitry, is a tumor suppressor miRNA implicated in the pathogenesis of CML and its clinical response to imatinib.
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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.