Dimethylsulfoxide induces upregulation of tumor suppressor protein PTEN through nuclear factor-κB activation in HL-60 cells

被引：25

作者：

Lee, YR

Shim, HJ

Yu, HN

Song, EK

Park, J

Kwon, KB

Park, JW

Rho, HW

Park, BH

Han, MK

Kim, JS ^{[1
]}

机构：

[1] Chonbuk Natl Univ, Sch Med, Dept Biochem, Chonju 560182, South Korea

[2] Chonbuk Natl Univ, Sch Med, Dept Microbiol & Immunol, Chonju 560182, South Korea

来源：

LEUKEMIA RESEARCH | 2005年 / 29卷 / 04期

关键词：

dimethylsulfoxide; PTEN; leukemic cell differentiation; NF-kappa B;

D O I：

10.1016/j.leukres.2004.09.010

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：401 / 405

页数：5

共 19 条

[1] The phosphoinositide 3-kinase/Akt pathway regulates cell cycle progression of HL60 human leukemia cells through cytoplasmic relocalization of the cyclin-dependent kinase inhibitor p27Kip1 and control of cyclin D1 expression [J].