Abstract:
:N-cadherin is a cell-cell adhesion molecule that plays a role in breast cancer metastasis. Here, we show that in vivo expression of N-cadherin in the PyMT mouse model, which enhances mammary tumor metastasis, results in selective inhibition of Akt3 expression and phosphorylation. Similarly, exogenous expression of N-cadherin in PyMT or MCF-7 mammary tumor cells enhanced cell motility and caused a dramatic reduction in Akt3 expression and phosphorylation. Moreover, knockdown of Akt3 in PyMT tumor cells increased cell motility and disrupted mammary morphogenesis, but had no effect on cell proliferation. Conversely, overexpression of wild-type Akt3 in PyMT-N-cadherin cells inhibited cell motility promoted by N-cadherin. Taken altogether, these findings demonstrate that N-cadherin suppresses Akt3 to promote cell motility and highlight the intricate regulation of Akt isoforms by N-cadherin during metastasis.
journal_name
Oncogenejournal_title
Oncogeneauthors
Chung S,Yao J,Suyama K,Bajaj S,Qian X,Loudig OD,Eugenin EA,Phillips GR,Hazan RBdoi
10.1038/onc.2012.65subject
Has Abstractpub_date
2013-01-24 00:00:00pages
422-30issue
4eissn
0950-9232issn
1476-5594pii
onc201265journal_volume
32pub_type
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