Revealing Genome-Wide mRNA and MicroRNA Expression Patterns in Leukemic Cells Highlighted HSA-MIR as a Tumor Suppressor for Regain of Chemotherapeutic Imatinib Response due to Targeting STAT5A

Kaymaz, Burcin TezcanliGunel, Nur SelviCeyhan, MetinCetintas, Vildan BozokOzel, BuketYandim, Melis KartalCan, Buket Kosova2025-09-252025-09-2520151010-42831423-0380https://doi.org/10.1007/s13277-015-3509-9https://hdl.handle.net/20.500.12573/4571Baran, Yusuf/0000-0002-1056-4673; Kartal Yandim, Melis/0000-0003-0573-4276; Ozel, Buket/0000-0003-2659-4129; Kipcak, Sezgi/0000-0003-0615-3844; Tezcanli Kaymaz, Burcin/0000-0003-1832-1454; Bozok, Vildan/0000-0003-3915-6363; Adan, Aysun/0000-0002-3747-8580BCR-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 mu M) 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 miRNAeninfo:eu-repo/semantics/openAccessImatinib ResistanceSTAT5AsiRNATranscriptome and miRNome ArrayApoptosisRevealing Genome-Wide mRNA and MicroRNA Expression Patterns in Leukemic Cells Highlighted HSA-MIR as a Tumor Suppressor for Regain of Chemotherapeutic Imatinib Response due to Targeting STAT5AArticle10.1007/s13277-015-3509-92-s2.0-84944280437