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Inhibition Of Cancer Cell Growth By Na/K‐ATPase Mimetic pNaKtide
Author(s) -
Li Zhichuan,
Lai Fangfang,
Xie Joe X,
Shapiro Joseph I,
Xie Zijian
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.932.6
Subject(s) - signal transduction , endocytosis , angiogenesis , cancer cell , cell growth , atpase , v atpase , cancer , microbiology and biotechnology , transduction (biophysics) , chemistry , apoptosis , cancer research , biology , cell , biochemistry , enzyme , genetics
Cells contain a large pool of non‐pumping Na/K‐ATPase that participates in signal transduction. Here, we show that the surface expression of Na/K‐ATPase is significantly reduced in human prostate carcinoma and cancer cell lines because of increased endocytosis. This down‐regulation impairs the ability of Na/K‐ATPase to regulate key signaling processes. Supplement of the Na/K‐ATPase or pNaKtide, a mimetic peptide derived from Na/K‐ATPase, normalizes the defective signal transduction. Consequently, these treatments stimulates apoptosis, inhibits growth and migration in cultures of 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 anti‐cancer therapeutics.