Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/2633
Title: Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells
Authors: Kosova, Buket
Tezcanlı, Burçin
Ekiz, Hüseyin Atakan
Çakır, Zeynep
Selvi, Nur
Dalmızrak, Ayşegül
Yandım, Melis Kartal
Gündüz, Ufuk
Baran, Yusuf
Ekiz, Hüseyin Atakan
Çakır, Zeynep
Yandım, Melis Kartal
Baran, Yusuf
Izmir Institute of Technology. Molecular Biology and Genetics
Keywords: siRNA knockdown
Reversal of resistance
Chronic myeloid leukemia
Small interfering RNA
STAT5A
Gene expression
Issue Date: Oct-2010
Publisher: Informa Healthcare
Source: 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
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.
URI: http://doi.org/10.3109/10428194.2010.507830
http://hdl.handle.net/11147/2633
ISSN: 1042-8194
1029-2403
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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