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

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KOSOVA B., Tezcanli B., Ekiz H. A., Cakir Z., SELVİ GÜNEL N., Dalmizrak A., ...More

LEUKEMIA & LYMPHOMA, vol.51, no.10, pp.1895-1901, 2010 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 51 Issue: 10
  • Publication Date: 2010
  • Doi Number: 10.3109/10428194.2010.507830
  • Journal Name: LEUKEMIA & LYMPHOMA
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.1895-1901
  • Keywords: Chronic myeloid leukemia (CML), chemotherapeutic resistance, reversal of resistance, imatinib, STAT5A, siRNA knockdown, CONSTITUTIVE ACTIVATION, LEUKEMIA-CELLS, PROTEINS, EXPRESSION, MECHANISM, PATHWAYS, LYMPHOMA, ROLES, LINES
  • Middle East Technical University Affiliated: Yes


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.