Dimethylsulfoxide induces upregulation of tumor suppressor protein PTEN through nuclear factor-κB activation in HL-60 cells
Dimethylsulfoxide induces upregulation of tumor suppressor protein PTEN through nuclear factor-κB activation in HL-60 cells
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DOI：
10.1016/j.leukres.2004.09.010
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发表时间：
2005-04-01
影响因子：
2.7
通讯作者：
Kim, JS
中科院分区：
文献类型：
--
作者：
Lee, YR;Shim, HJ;Kim, JS
二甲基亚砜(DMSO)可诱导HL60细胞分化为中性粒细胞样细胞。在此，我们提供了肿瘤抑制基因PTEN参与DMSO诱导HL60细胞分化的证据，PTEN是磷脂酰肌醇3-激酶(PI3K)的拮抗剂。DMSO上调PTEN的表达，但不影响PI3K的表达。DMSO上调PTEN表达导致PI3K下游Akt磷酸化水平降低。DMSO诱导的PTEN上调可能是通过激活核因子-kB介导的，核因子-kappaB抑制剂吡咯烷二硫代氨基甲酸酯(PDTC)阻断了DMSO诱导的PTEN上调。(C)2004爱思唯尔有限公司。保留所有权利。
Dimethylsulfoxide (DMSO) has been known to differentiate HL60 cells into neutrophil like cells. Here, we provide an evidence for the involvement of tumor suppressor PTEN, an antagonist of phosphatidylinositol 3-kinase (PI3K) in the DMSO-induced differentiation of HL60 cells. DMSO upregulated PTEN with unaffecting the expression of PI3K. The upregulation of PTEN by DMSO lead to the decrease of Akt phosphorylation, a downstream of PI3K. The DMSO-induced upregulation of PTEN might be mediated by NF-KB activation, which was evidenced by the blockage of DMSO-induced PTEN upregulation with an NF-kappa B inhibitor, pyrrolidine dithiocarbamate (PDTC). (c) 2004 Elsevier Ltd. All rights reserved.