mir-188-5p emerges as an oncomir to promote chronic myeloid leukemia via upregulation of BUB3 and SUMO2

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dc.authoridPetrovic, Nina/0000-0003-2503-1228
dc.contributor.authorAkidan, Osman
dc.contributor.authorPetrovic, Nina
dc.contributor.authorMisir, Sema
dc.date.accessioned2025-05-04T16:47:25Z
dc.date.available2025-05-04T16:47:25Z
dc.date.issued2025
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractBackgroundChronic 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.
dc.identifier.doi10.1007/s11033-025-10359-9
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.issue1
dc.identifier.pmid40019654
dc.identifier.scopus2-s2.0-85219593630
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1007/s11033-025-10359-9
dc.identifier.urihttps://hdl.handle.net/20.500.12418/35607
dc.identifier.volume52
dc.identifier.wosWOS:001434940400001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofMolecular Biology Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250504
dc.subjectChronic myeloid leukemia
dc.subjectmiR-188-5p
dc.subjectBUB3
dc.subjectSUMO2
dc.titlemir-188-5p emerges as an oncomir to promote chronic myeloid leukemia via upregulation of BUB3 and SUMO2
dc.typeArticle

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