Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells

• Published in: Leukemia & lymphoma Vol. 51; no. 10; pp. 1895 - 1901
• Main Authors: Kosova, Buket, Tezcanli, Burcin, Ekiz, Huseyin Atakan, Cakir, Zeynep, Selvi, Nur, Dalmizrak, Aysegul, Kartal, Melis, Gunduz, Ufuk, Baran, Yusuf
• Format: Journal Article
• Language: English
• Published: United States Informa Healthcare 01.10.2010; Taylor & Francis
• Subjects: Antineoplastic Agents - pharmacology; Apoptosis - drug effects; Apoptosis - genetics; Benzamides; Caspase 3 - metabolism; Cell Proliferation - drug effects; Cell Survival - drug effects; Cell Survival - genetics; chemotherapeutic resistance; Chronic myeloid leukemia (CML); Dose-Response Relationship, Drug; Drug Resistance, Neoplasm; Enzyme Activation - drug effects; Gene Expression Profiling; Gene Expression Regulation, Leukemic; Humans; Imatinib Mesylate; imatinib, STAT5A; K562 Cells; Piperazines - pharmacology; Pyrimidines - pharmacology; reversal of resistance; Reverse Transcriptase Polymerase Chain Reaction; RNA Interference; siRNA knockdown; STAT3 Transcription Factor - genetics; STAT5 Transcription Factor - genetics; Tumor Suppressor Proteins - genetics
• ISSN: 1042-8194; 1029-2403
• DOI: 10.3109/10428194.2010.507830

STAT proteins are cytoplasmic transcription factors that are involved in the regulation of numerous cellular activities such as cell growth, differentiation, and survival. In this study, we aimed to identify the expression pattern of STAT genes in imatinib-sensitive and -resistant K562 cells, and further, to reveal the effects of STAT5A siRNA knockdown on cell growth and apoptosis induction. The XTT cell proliferation assay showed that both sensitive and resistant K562 cells were sensitized to imatinib upon transfection with STAT5A siRNA. Caspase-3 enzyme activity was increased significantly in both cells. These results may open up new opportunities to overcome chemotherapeutic resistance in leukemia.