Suppression of Stat5a Increases Chemotherapeutic Sensitivity in Imatinib-Resistant and Imatinib-Sensitive K562 Cells

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BRONZE

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Yes

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6

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Abstract

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. © 2010 Informa UK, Ltd.

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Keywords

siRNA knockdown, Reversal of resistance, Chronic myeloid leukemia, Small interfering RNA, STAT5A, Gene expression, STAT3 Transcription Factor, Cell Survival, Antineoplastic Agents, Apoptosis, Piperazines, Chronic myeloid leukemia (CML), Reversal of resistance, STAT5 Transcription Factor, chemotherapeutic resistance, Humans, siRNA knockdown, Cell Proliferation, Dose-Response Relationship, Drug, Caspase 3, Gene Expression Regulation, Leukemic, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Chronic myeloid leukemia, Small interfering RNA, Enzyme Activation, STAT5A, Pyrimidines, imatinib, Drug Resistance, Neoplasm, Benzamides, Imatinib Mesylate, RNA Interference, Gene expression, K562 Cells, reversal of resistance

Fields of Science

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

Citation

Kosova, B., Tezcanlı, B., Ekiz, H. A., Çakır, Z., Selvi, N., Dalmızrak, A., Kartal, M., Gündüz, U., and Baran, Y. (2010). Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells. Leukemia and Lymphoma, 51(10), 1895-1901. doi:10.3109/10428194.2010.507830

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18

Volume

51

Issue

10

Start Page

1895

End Page

1901
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Scopus : 16

PubMed : 9

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