Akt isoform-specific inhibition of MDA-MB-231 cell proliferation
- Authors
- Yang, Wonseok; Ju, Ji-hyun; Lee, Kyung-min; Shin, Incheol
- Issue Date
- Jan-2011
- Publisher
- ELSEVIER SCIENCE INC
- Keywords
- Akt isoforms; Breast cancer; CDK2; ERK; p27
- Citation
- CELLULAR SIGNALLING, v.23, no.1, pp.19 - 26
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELLULAR SIGNALLING
- Volume
- 23
- Number
- 1
- Start Page
- 19
- End Page
- 26
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/169271
- DOI
- 10.1016/j.cellsig.2010.07.016
- ISSN
- 0898-6568
- 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.
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