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二甲基亚砜通过激活核因子-κB诱导HL-60细胞中肿瘤抑制蛋白PTEN的上调。

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

作者信息

Lee Young-Rae, Shim Hyun-Jaung, Yu Hong-Nu, Song Eun-Kyung, Park Jinny, Kwon Kang-Beom, Park Jin-Woo, Rho Hye-Won, Park Byung-Hyun, Han Myung-Kwan, Kim Jong-Suk

机构信息

Department of Biochemistry, Chonbuk National University Medical School, Chonju 560-182, Republic of Korea.

出版信息

Leuk Res. 2005 Apr;29(4):401-5. doi: 10.1016/j.leukres.2004.09.010. Epub 2005 Jan 12.

Abstract

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-kappaB activation, which was evidenced by the blockage of DMSO-induced PTEN upregulation with an NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC).

摘要

二甲基亚砜(DMSO)已知可将HL60细胞分化为中性粒细胞样细胞。在此,我们提供证据表明肿瘤抑制因子PTEN(磷脂酰肌醇3激酶(PI3K)的拮抗剂)参与了DMSO诱导的HL60细胞分化过程。DMSO上调了PTEN,而不影响PI3K的表达。DMSO对PTEN的上调导致PI3K下游的Akt磷酸化水平降低。DMSO诱导的PTEN上调可能由NF-κB激活介导,这一点可通过用NF-κB抑制剂吡咯烷二硫代氨基甲酸盐(PDTC)阻断DMSO诱导的PTEN上调来证明。

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