Document Type

Article

Publication Date

Summer 7-22-2011

Abstract

Cells contain a large pool of non-pumping Na/K-ATPase that participates in signal transduction. Here, we show that the expression of α1 Na/K-ATPase is significantly reduced in human prostate carcinoma as well as in several human cancer cell lines. This down-regulation impairs the ability of Na/K-ATPase to regulate Src-related signaling processes. Supplement of pNaKtide, a peptide derived from α1 Na/K-ATPase, reduces activities of Src and Src effectors. Consequently, these treatments stimulate apoptosis and inhibit growth in cultures of human cancer cells. Moreover, administration of pNaKtide inhibits angiogenesis and growth of tumor xenograft. Thus, the new findings demonstrate the in vivo effectiveness of pNaKtide, and suggest that the defect in Na/K-ATPase-mediated signal transduction may be targeted for developing new anti-cancer therapeutics.

Comments

The version of record is available from the publisher at http://www.jbc.org/content/286/37/32394.full.pdf+html. This research was originally published in The Journal of Biological Chemistry. Li Z, Z Zhang, JX Xie, X Li, J Tian, T Cai, H Cui, H Ding, JI Shapiro and Z Xie. Na/K-ATPase mimetic pNaKtide peptide inhibits the growth of human cancer cells. Journal of Biological Chemistry. 2011; 286:32394-32403. © the American Society for Biochemistry and Molecular Biology. Reprinted with permission. All rights reserved. DOI 10.1074/jbc.M110.207597

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