Suppression of STAT5A and STAT5B chronic myeloid leukemia cells via siRNA and antisense-oligonucleotide applications with the induction of apoptosis

American Journal of Blood Research

Vildan Bozok Çetintaş¹  Fahri Şahin¹  Buket Kosova¹  Burçin Tezcanlı Kaymaz¹  Yusuf Baran¹  Çağdaş Aktan¹  Nur Selvi¹  Aysun Adan Gokbulut¹  Güray Saydam¹  Cumhur Gündüz¹ 

关键词: Chronic myeloid leukemia;    K562;    STAT5;    siRNA knockdown;    antisense oligonucleotides;    apoptosis;   

DOI  :  

学科分类：血液学

来源: e-Century Publishing Corporation

【 摘 要 】

Signal transducers and activators of transcription (STAT) proteins function in the JAK/STAT signaling pathway and are activated by phosphorylation. As a result of this signaling event, they affect many cellular processes including cell growth, proliferation, differentiation, and survival. Increases in the expressions of STAT5A and STAT5B play a remarkable role in the development of leukemia in which leukemic cells gain uncontrolled proliferation and angiogenesis ability. At the same time, these cells acquire ability to escape from apoptosis and host immune system. In this study, we aimed to suppress STAT-5A and -5B genes in K562 CML cells by siRNA transfection and antisense oligonucleotides (ODN) targeting and then to evaluate apoptosis rate. Finally, we compared the transfection efficiencies of these approaches. Quantitative RT-PCR and Western blot results indicated that STAT expressions were downregulated at both mRNA and protein levels following siRNA transfection. However, electroporation mediated ODN transfection could only provide limited suppression rates at mRNA and protein levels. Moreover, it was displayed that apoptosis were significantly induced in siRNA treated leukemic cells as compared to ODN treated cells. As a conclusion, siRNA applications were found to be more effective in terms of gene silencing when compared to ODN treatment based on the higher apoptosis and mRNA suppression rates. siRNA application could be a new and alternative curative method as a supporting therapy in CML patients.

【 授权许可】

Unknown