Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/5916
Title: Revealing genome-wide mRNA and microRNA expression patterns in leukemic cells highlighted “hsa-miR-2278” as a tumor suppressor for regain of chemotherapeutic imatinib response due to targeting STAT5A
Authors: Tezcanlı Kaymaz, Burçin
Selvi Günel, Nur
Ceyhan, Metin
Bozok Çetintaş, Vildan
Özel, Buket
Kartal Yandım, Melis
Kıpçak, Sezgi
Aktan, Çağdaş
Adan Gökbulut, Aysun
Baran, Yusuf
Kosova Can, Buket
Keywords: Apoptosis
Imatinib resistance
siRNA
STAT5A
Transcriptome and miRNome array
Chronic myeloid leukemia
MicroRNAs
Issue Date: Sep-2015
Publisher: SAGE Publications Inc.
Source: Tezcanlı Kaymaz, B., Selvi Günel, N., Ceyhan, M., Bozok Çetintaş, V., Özel, B., Kartal Yandım, M., Kıpçak, S., Aktan, Ç., Adan Gökbulut, A., Baran, Y., and Kosova Can, B. (2015). Revealing genome-wide mRNA and microRNA expression patterns in leukemic cells highlighted “hsa-miR-2278” as a tumor suppressor for regain of chemotherapeutic imatinib response due to targeting STAT5A. Tumor Biology, 36(10), 7915-7927. doi:10.1007/s13277-015-3509-9
Abstract: BCR-ABL oncoprotein stimulates cell proliferation and inhibits apoptosis in chronic myeloid leukemia (CML). For cure, imatinib is a widely used tyrosine kinase inhibitor, but developing chemotherapeutic resistance has to be overcome. In this study, we aimed to determine differing genome-wide microRNA (miRNA) and messenger RNA (mRNA) expression profiles in imatinib resistant (K562/IMA-3 μM) and parental cells by targeting STAT5A via small interfering RNA (siRNA) applications. After determining possible therapeutic miRNAs, we aimed to check their effects upon cell viability and proliferation, apoptosis, and find a possible miRNA::mRNA interaction to discover the molecular basis of imatinib resistance. We detected that miR-2278 and miR-1245b-3p were most significantly regulated miRNAs according to miRNome array. Upregulating miR-2278 expression resulted in the inhibition of resistant leukemic cell proliferation and induced apoptosis, whereas miR-1245b-3p did not exhibit therapeutic results. Functional analyses indicated that AKT2, STAM2, and STAT5A mRNAs were functional targets for miR-2278 as mimic transfection decreased their expressions both at transcriptional and translational level, thus highlighting miR-2278 as a tumor suppressor. This study provides new insights in discovering the mechanism of imatinib resistance due to upregulating the tumor-suppressor hsa-miR-2278 which stands for a functional therapeutic approach, inhibited leukemic cell proliferation, induced apoptosis, and regain of chemotherapeutic drug response in CML therapy. © 2015, International Society of Oncology and BioMarkers (ISOBM).
URI: http://doi.org/10.1007/s13277-015-3509-9
http://hdl.handle.net/11147/5916
ISSN: 1423-0380
1010-4283
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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