CIP2A is over-expressed in acute myeloid leukaemia and associated with HL60 cells proliferation and differentiation
CIP2A is over-expressed in acute myeloid leukaemia and associated with HL60 cells proliferation and differentiation
复制标题
CIP2A 在急性髓系白血病中过度表达并与 HL60 细胞增殖和分化相关
DOI：
10.1111/j.1751-553x.2010.01288.x
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发表时间：
2011-06-01
影响因子：
3
通讯作者：
Chen, C.
中科院分区：
文献类型：
--
作者：
Wang, J.;Li, W.;Chen, C.
CIP2A是一种新发现的PP2A抑制剂。它可以稳定c-Myc，促进非锚定细胞生长和肿瘤形成。CIP2A在一些实体肿瘤中过表达，尽管其在急性髓性白血病（AML）中的表达尚不清楚。方法：分别采用逆转录聚合酶链反应和Western blot检测AML患者和健康对照者骨髓单个核细胞中CIP2A mRNA和蛋白的表达。我们使用siRNA敲除HL60细胞中CIP2A的表达，然后检测其在AML病理进展中的潜在作用。结果：70例新诊断AML患者中有54例（77.14%）存在CIP2A mRNA， 14例复发AML患者中有11例（70.86%）存在CIP2A mRNA，显著高于完全缓解标本和健康对照组（P < 0.001）。在HL60细胞中敲低CIP2A可减缓细胞增殖，降低克隆活性，促进细胞分化。结论：这些结果表明CIP2A在新诊断/复发的AML患者中过表达，CIP2A的表达可能作为AML治疗后复发的临床标志物。CIP2A在HL60细胞中的高表达可能与激活细胞增殖和抑制细胞分化有关。本研究可能揭示CIP2A在髓性白血病发生中的分子功能。
P>Introduction:CIP2A is a newly identified inhibitor of PP2A. It can stabilize c-Myc and promote anchorage-independent cell growth and tumour formation. CIP2A is over-expressed in some solid tumours although its expression in acute myeloid leukaemia (AML) is still unknown.Methods:CIP2A mRNA and protein expressions were determined in bone marrow mononuclear cells of both patients with AML and healthy controls using reverse transcription polymerase chain reaction and Western blot, respectively. We used siRNA to knock-down CIP2A expression in HL60 cells and then examined its potential roles during the pathological progression of AML.Results:CIP2A mRNA was present in 54 of 70 (77.14%) patients with newly diagnosed AML and in 11 of 14 (70.86%) patients with relapsed AML, which was significantly higher than complete remission specimens and healthy controls (P < 0.001). Knock-down of CIP2A in HL60 cells slowed down cell proliferation, decreased clonogenic activity and promoted cell differentiation.Conclusion:These results suggest that CIP2A is over-expressed in patients with newly diagnosed/relapsed AML and the expression of CIP2A could have potential use as a clinical marker for AML relapse after treatment. The high expression of CIP2A in HL60 cells may be related to active cell proliferation and arrest of cell differentiation. This study may shed light on the molecular function of CIP2A in myeloid leukemogenesis.