首页> 外文期刊>Leukemia and lymphoma >Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells.
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Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells.

机译:STAT5A的抑制可提高伊马替尼耐药和伊马替尼敏感的K562细胞的化疗敏感性。

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摘要

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.
机译:STAT蛋白是细胞质转录因子,参与许多细胞活动(如细胞生长,分化和存活)的调控。在这项研究中,我们旨在确定STAT基因在对伊马替尼敏感和耐药的K562细胞中的表达模式,并进一步揭示STAT5A siRNA敲低对细胞生长和凋亡诱导的影响。 XTT细胞增殖试验表明,在用STAT5A siRNA转染后,敏感和耐药K562细胞均对伊马替尼敏感。在两个细胞中,Caspase-3酶的活性均显着增加。这些结果可能为克服白血病的化疗耐药性提供新的机会。

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