ArticleMolecular biology reports2025
mir-188-5p emerges as an oncomir to promote chronic myeloid leukemia via upregulation of BUB3 and SUMO2.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Candidate Regulatory Relationship and Expression Correlation Between miR-33a-5p and ANK3 in Chronic Myeloid Leukemia.Current issues in molecular biology · 2026Article
- The biology of chronic myeloid leukemia: an overview of the new insights and biomarkers.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic myeloid leukemia (CML) is an aggressive malignancy originating from hematopoietic stem cells. miRNAs play a role in physiological and developmental processes, including cellular proliferation, apoptosis, angiogenesis, and differentiation, and in CML's prognosis, diagnosis, and treatment. This study aimed to investigate the function and possible mechanisms of action of miR-188-5p in the development and progression of chronic myeloid leukemia. METHODS AND
resultsmiRNA expression profiles were obtained from the GSE90773 dataset in the Gene Expression Omnibus (GEO). GEO2R was used to identify differentially expressed miRNAs. miRNET, miRDB, CancerSEA, GeneMANIA, and BioGRID databases were applied to assess the biological function of miRNA and target molecules in CML. RT-PCR performed validation analyses of miRNA and target molecules in CML. To determine the power of miR-188-5p expression levels to distinguish patients with CML from control, the ROC analysis was performed. miR-188-5p is significantly increased in K-562 cells, and overexpression of miR-188-5p was associated with clinicopathological features. miR-188-5p showed significantly higher AUC values (AUC = 1.0, p = 0.0001). The cut-off of miR-188-5p was 6.74. miRDB and mirNET predicted BUB3 and SUMO2 as a potential target gene of miR-188-5p. Additionally, increased expression of BUB3 and SUMO2 was observed in the K-562 cell. Bub3 is implicated in apoptosis and the cell cycle, whereas Sumo2 protein sumoylation and DNA binding are believed to contribute to catabolic processes.
conclusionsOur results suggest that miR-188-5p acts as an oncomiRNA in CML pathogenesis and may be a promising therapeutic target for CML.
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Registered trials
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