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

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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 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 miRNA

Description

Baran, 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/0000-0002-3747-8580

Keywords

Imatinib Resistance, STAT5A, siRNA, Transcriptome and miRNome Array, Apoptosis, Transcriptome andmiRNome Array, Blotting, Western, Apoptosis, Real-Time Polymerase Chain Reaction, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Biomarkers, Tumor, STAT5 Transcription Factor, Tumor Cells, Cultured, Humans, RNA, Messenger, Imatinib resistance, RNA, Small Interfering, Protein Kinase Inhibitors, Cell Proliferation, Oligonucleotide Array Sequence Analysis, Gene Expression Regulation, Leukemic, Genome, Human, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Chronic myeloid leukemia, Transcriptome and miRNome array, STAT5A, MicroRNAs, Drug Resistance, Neoplasm, siRNA, Imatinib Mesylate

Fields of Science

0301 basic medicine, 03 medical and health sciences, 0303 health sciences

Citation

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OpenCitations Citation Count
27

Volume

36

Issue

10

Start Page

7915

End Page

7927