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首页> 外文期刊>Clinical cancer research: an official journal of the American Association for Cancer Research >HDAC Inhibition Induces MicroRNA-182, which Targets RAD51 and Impairs HR Repair to Sensitize Cells to Sapacitabine in Acute Myelogenous Leukemia
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HDAC Inhibition Induces MicroRNA-182, which Targets RAD51 and Impairs HR Repair to Sensitize Cells to Sapacitabine in Acute Myelogenous Leukemia

机译:HDAC抑制诱导MicroRNA-182,其靶向RAD51并损害HR修复以敏化急性粒细胞性白血病中的细胞对沙巴他滨

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摘要

Purpose: The double-strand breaks elicited by sapacitabine, a clinically active nucleoside analogue prodrug, are repaired by RAD51 and the homologous recombination repair (HR) pathway, which could potentially limit its toxicity. We investigated the mechanism by which histone deacetylase (HDAC) inhibitors targeted RAD51 and HR to sensitize acute myelogenous leukemia (AML) cells to sapacitabine.
机译:目的:由RAD51和同源重组修复(HR)途径修复由具有临床活性的核苷类似物前药sapacitabine引起的双链断裂,这可能会限制其毒性。我们研究了组蛋白脱乙酰基酶(HDAC)抑制剂针对RAD51和HR致敏急性粒细胞性白血病(AML)细胞对沙巴他滨敏感的机制。

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