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

Title
Akt isoform-specific inhibition of MDA-MB-231 cell proliferation
Author
신인철
Keywords
Akt isoforms; Breast cancer; CDK2; ERK; p27; PROTEIN-KINASE-B; EPITHELIAL-MESENCHYMAL TRANSITION; GLUCOSE-HOMEOSTASIS; MICE LACKING; CYCLE PROGRESSION; DOWN-REGULATION; DISTINCT ROLES; HUMAN CANCER; IN-VITRO; PATHWAY
Issue Date
2011-01
Publisher
ELSEVIER SCIENCE INC, 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
Citation
Cellular signalling, Vol.23 No.1 [2011], 19-26
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. (C) 2010 Elsevier Inc. All rights reserved.
URI
http://www.sciencedirect.com/science/article/pii/S0898656810002093?via%3Dihubhttp://hdl.handle.net/20.500.11754/66118
ISSN
0898-6568
DOI
10.1016/j.cellsig.2010.07.016
Appears in Collections:
COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > Articles
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