血管扩张剂和利钾尿肽抑制人前列腺癌细胞中MEK 1/2的激活。

Vessel dilator and kaliuretic peptide inhibit MEK 1/2 activation in human prostate cancer cells.

作者信息

Sun Ying, Eichelbaum Ehrentraud J, Wang Hai, Vesely David L

机构信息

Department of Internal Medicine, University of South Florida Cardiac Hormone Center and James A. Haley Veterans Medical Center, Tampa, Florida 33612, USA.

出版信息

Anticancer Res. 2007 May-Jun;27(3B):1387-92.

PMID:17595752

Abstract

BACKGROUND

Vessel dilator and kaliuretic peptide have anticancer effects in human prostate adenocarcinomas.

MATERIALS AND METHODS

The effect of vessel dilator, kaliuretic peptide and cyclic GMP on MEK 1/2 kinase were examined in human prostate adenocarcinoma cells.

RESULTS

Vessel dilator and kaliuretic peptide decreased the activation of MEK 1/2 over a concentration range of 0.01 microM to 10 microM. Vessel dilator and kaliuretic peptide (each 10 microM) inhibited the phosphorylation of MEK 1/2 kinase by 98% (p < 0.0001) and 81% (p < 0.001), respectively. The inhibition of MEK 1/2 lasted for at least two hours, where it was maximal, secondary to both peptides. Their ability to inhibit MEK 1/2 was inhibited by cyclic GMP antibody and cyclic GMP itself inhibited MEK 1/2 phosphorylation.

CONCLUSION

Vessel dilator and kaliuretic peptide both inhibit MEK 1/2 kinase mediated via cyclic GMP as part of their anticancer mechanism(s) of action.

摘要

背景

血管舒张肽和利钾尿肽对人前列腺腺癌具有抗癌作用。

材料与方法

在人前列腺腺癌细胞中检测血管舒张肽、利钾尿肽和环磷酸鸟苷对MEK 1/2激酶的作用。

结果

在0.01微摩尔至10微摩尔的浓度范围内，血管舒张肽和利钾尿肽降低了MEK 1/2的活性。血管舒张肽和利钾尿肽（各10微摩尔）分别使MEK 1/2激酶的磷酸化抑制了98%（p < 0.0001）和81%（p < 0.001）。MEK 1/2的抑制作用持续至少两小时，在此期间达到最大值，这是两种肽共同作用的结果。它们抑制MEK 1/2的能力被环磷酸鸟苷抗体抑制，且环磷酸鸟苷本身也抑制MEK 1/2的磷酸化。