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Cell Signal. 2011 Jan;23(1):19-26. doi: 10.1016/j.cellsig.2010.07.016. Epub 2010 Aug 2.

Akt isoform-specific inhibition of MDA-MB-231 cell proliferation.

Author information

1
Dept. of Life Science, Hanyang University, Seoul, Korea.

Abstract

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.

PMID:
20688159
DOI:
10.1016/j.cellsig.2010.07.016
[Indexed for MEDLINE]

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