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

• DOI: 10.1007/s13277-015-3509-9
• Publication Date: 2015-05-07T20:46:10Z
• Authors: Burçin Tezcanlı K...; Nur Selvi Günel; Metin Ceyhan; Vildan Bozok Çeti...; Buket Özel; Melis Kartal Yandım; Sezgi Kıpçak; Çağdaş Aktan; Aysun Adan Gökbulut; Yusuf Baran; Buket Kosova Can
• Keywords: Imatinib Mesylate; K562 cells

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 determine differing genome-wide microRNA (miRNA) messenger RNA (mRNA) expression profiles resistant (K562/IMA-3 μM) parental cells by targeting STAT5A via small interfering (siRNA) applications. After determining possible therapeutic miRNAs, check their effects upon viability proliferation, apoptosis, find miRNA::mRNA interaction discover the molecular basis of resistance. We detected that miR-2278 miR-1245b-3p were most significantly regulated miRNAs according miRNome array. Upregulating resulted inhibition leukemic induced whereas did not exhibit results. Functional analyses indicated AKT2, STAM2, mRNAs functional targets for as mimic transfection decreased expressions both at transcriptional translational level, thus highlighting tumor suppressor. This study provides new insights discovering mechanism due upregulating tumor-suppressor hsa-miR-2278 which stands approach, inhibited regain drug response CML therapy.