Journal
CELLULAR SIGNALLING
Volume 23, Issue 1, Pages 19-26Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2010.07.016
Keywords
Akt isoforms; Breast cancer; CDK2; ERK; p27
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Funding
- Ministry of Welfare and Family Affairs [A084466]
- Korean Ministry of Science and Technology [FPR09A2-080]
- Korea Science and Engineering Foundation [2008-05943]
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To dissect the isoform-specific roles of Akt in breast cancer cells, constitutively active Akt isoforms were introduced into MDA-MB-231 cells. Both Akt1 and Akt2 efficiently inhibited the growth of MDA-MB-231 cells. Overexpression of Akt1 down-regulated ERK activity inhibiting Ser 259 phosphorylation of c-Raf and subsequent downstream signaling. Akt2 overexpression up-regulated the cell cycle inhibitor p27. Cycloheximide decay assays showed that Akt2 increased the stability and nuclear localization of p27, thus inhibiting the cyclin E/CDK2 complex. These results suggest that the inhibition of cell proliferation by Akt1 and Akt2 is mediated by isoform-specific mechanisms. (C) 2010 Elsevier Inc. All rights reserved.
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