Akt isoform-specific inhibition of MDA-MB-231 cell proliferation
Copyright policy )Akt isoform-specific inhibition of MDA-MB-231 cell proliferation
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.
- Hanyang University Korea (Republic of)
Cyclin-Dependent Kinase 2, Breast Neoplasms, Protein Structure, Tertiary, Proto-Oncogene Proteins c-raf, Cell Line, Tumor, Cyclin E, Humans, Protein Isoforms, Female, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Proto-Oncogene Proteins c-akt, Cyclin-Dependent Kinase Inhibitor p27, Cell Proliferation, Signal Transduction
Cyclin-Dependent Kinase 2, Breast Neoplasms, Protein Structure, Tertiary, Proto-Oncogene Proteins c-raf, Cell Line, Tumor, Cyclin E, Humans, Protein Isoforms, Female, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Proto-Oncogene Proteins c-akt, Cyclin-Dependent Kinase Inhibitor p27, Cell Proliferation, Signal Transduction
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