| Literature DB >> 35059859 |
Cagla Kayabasi1, Ayse Caner2,3, Sunde Yilmaz Susluer4, Tugce Balci Okcanoglu5, Besra Ozmen Yelken6, Aycan Asik4, Zeynep Mutlu4, Cansu Caliskan Kurt4, Bakiye Goker Bagca7, Cigir Biray Avci4, Fahri Sahin8, Guray Saydam8, Cumhur Gunduz4.
Abstract
LncRNAs are associated with malignancies with their tumor suppressor/oncogenic properties. Although many studies are conducted related to the mechanism of action for dasatinib and ponatinib in chronic myeloid leukemia (CML), their comparative effects on lncRNA expressions are largely unknown. Hence, we aimed to define the lncRNAs involved in the treatment of CML with dasatinib and ponatinib. We measured the cytotoxicities of dasatinib/ponatinib with CCK-8 assay and identified differentially expressed lncRNAs (DEL) by qRT-PCR. We determined the principal functions of DELs by Ingenuity Pathway Analysis (IPA) and performed gene ontology (GO) analysis for apoptosis and anti-proliferation-related lncRNAs. Apoptotic and anti-proliferative activities of dasatinib/ponatinib were confirmed by flow-cytometry. In K562 cells, dasatinib/ponatinib re-regulated lncRNAs which were dysregulated in leukemia. DELs after treatment (forty with dasatinib, thirty-seven with ponatinib) were related to increased cell death; decreased cell viability, proliferation, tumor growth, invasion, migration. Dasatinib-mediated network was related to cancer, hematological disease while ponatinib-mediated network was associated with cancer, cell death/survival, cell-to-cell signaling/interaction. Both treatments predicted activation of IFNγ, IL1β, TNF as upstream regulators, specially this effect was higher in dasatinib. Comparison analysis showed that ponatinib was predicted more effective in cell death of tumor cell line than dasatinib. We confirmed that ponatinib was more potent than dasatinib to induce apoptosis and inhibit proliferation of CML cells, in consensus with IPA and GO analysis results. LncRNAs are specifically involved in anti-leukemic activities of dasatinib and ponatinib. Our findings will contribute to understanding signalization occurring in CML cells after standard treatments.Entities:
Keywords: Cell death; Cell proliferation; Chronic myeloid leukemia; Ingenuity pathway analysis; Long non-coding RNA; Tyrosine kinase inhibitors
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Year: 2022 PMID: 35059859 DOI: 10.1007/s12032-021-01629-0
Source DB: PubMed Journal: Med Oncol ISSN: 1357-0560 Impact factor: 3.064