Sun Ying, Eichelbaum Ehrentraud J, Wang Hai, Vesely David L
Department of Internal Medicine, University of South Florida Cardiac Hormone Center and James A. Haley Veterans Medical Center, Tampa, Florida 33612, USA.
Anticancer Res. 2007 May-Jun;27(3B):1387-92.
Vessel dilator and kaliuretic peptide have anticancer effects in human prostate adenocarcinomas.
The effect of vessel dilator, kaliuretic peptide and cyclic GMP on MEK 1/2 kinase were examined in human prostate adenocarcinoma cells.
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.
Vessel dilator and kaliuretic peptide both inhibit MEK 1/2 kinase mediated via cyclic GMP as part of their anticancer mechanism(s) of action.
血管舒张肽和利钾尿肽对人前列腺腺癌具有抗癌作用。
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。
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。
血管舒张肽和利钾尿肽均通过环磷酸鸟苷介导抑制MEK 1/2激酶，这是它们抗癌作用机制的一部分。
