Induction of E-cadherin endocytosis by loss of protein phosphatase 2A expression in human breast cancers

2006 ◽  
Vol 349 (1) ◽  
pp. 255-260 ◽  
Author(s):  
Katsuo Suzuki ◽  
Kazuhide Takahashi
2000 ◽  
Vol 93 (1-2) ◽  
pp. 83-93 ◽  
Author(s):  
Jürgen Götz ◽  
Alphonse Probst ◽  
Claudia Mistl ◽  
Roger M Nitsch ◽  
Elisabeth Ehler

2005 ◽  
Vol 280 (43) ◽  
pp. 35829-35835 ◽  
Author(s):  
Li Hui ◽  
Vanessa Rodrik ◽  
Rafal M. Pielak ◽  
Stefan Knirr ◽  
Yang Zheng ◽  
...  

A critical aspect of tumor progression is the generation of survival signals that overcome default apoptotic programs. Recent studies have revealed that elevated phospholipase D activity generates survival signals in breast and perhaps other human cancers. We report here that the elevated phospholipase D activity in the human breast cancer cell line MDA-MB-231 suppresses the activity of the putative tumor suppressor protein phosphatase 2A in a mammalian target of rapamycin (mTOR)-dependent manner. Increasing the phospholipase D activity in MCF7 cells also suppressed protein phosphatase 2A activity. Elevated phospholipase D activity suppressed association of protein phosphatase 2A with both ribosomal subunit S6-kinase and eukaryotic initiation factor 4E-binding protein 1. Suppression of protein phosphatase 2A by SV40 small t-antigen has been reported to be critical for the transformation of human cells with SV40 early region genes. Consistent with a critical role for protein phosphatase 2A in phospholipase D survival signals, either SV40 small t-antigen or pharmacological suppression of protein phosphatase 2A restored survival signals lost by the suppression of either phospholipase D or mTOR. Blocking phospholipase D signals also led to reduced phosphorylation of the pro-apoptotic protein BAD at the protein phosphatase 2A dephosphorylation site at Ser-112. The ability of phospholipase D to suppress protein phosphatase 2A identifies a critical target of an emerging phospholipase D/mTOR survival pathway in the transformation of human cells.


2017 ◽  
Vol 38 (1) ◽  
pp. 598-606 ◽  
Author(s):  
Qiuyue Huang ◽  
Shanshan Qin ◽  
Xiaoning Yuan ◽  
Liang Zhang ◽  
Juanli Ji ◽  
...  

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