δ-Tocopherol inhibits receptor tyrosine kinase-induced AKT activation in prostate cancer cells

2015 ◽  
Vol 55 (11) ◽  
pp. 1728-1738 ◽  
Author(s):  
Hong Wang ◽  
Jungil Hong ◽  
Chung S. Yang
BMC Cancer ◽  
2015 ◽  
Vol 15 (1) ◽  
Author(s):  
Inga Mertens-Walker ◽  
Bruno C Fernandini ◽  
Mohanan SN Maharaj ◽  
Anja Rockstroh ◽  
Colleen C Nelson ◽  
...  

2014 ◽  
Vol 50 ◽  
pp. S122-S123
Author(s):  
A. Herington ◽  
I. Mertens-Walker ◽  
B. Fernandini ◽  
A. Rockstroh ◽  
C. Nelson ◽  
...  

Oncotarget ◽  
2015 ◽  
Vol 6 (17) ◽  
pp. 15321-15331 ◽  
Author(s):  
Nitu Bansal ◽  
Prasun J. Mishra ◽  
Mark Stein ◽  
Robert S. DiPaola ◽  
Joseph R. Bertino

2015 ◽  
Vol 26 (11) ◽  
pp. 1971-1984 ◽  
Author(s):  
Julia Lindqvist ◽  
Susumu Y. Imanishi ◽  
Elin Torvaldson ◽  
Marjo Malinen ◽  
Mika Remes ◽  
...  

Contrary to cell cycle–associated cyclin-dependent kinases, CDK5 is best known for its regulation of signaling processes in differentiated cells and its destructive activation in Alzheimer's disease. Recently, CDK5 has been implicated in a number of different cancers, but how it is able to stimulate cancer-related signaling pathways remains enigmatic. Our goal was to study the cancer-promoting mechanisms of CDK5 in prostate cancer. We observed that CDK5 is necessary for proliferation of several prostate cancer cell lines. Correspondingly, there was considerable growth promotion when CDK5 was overexpressed. When examining the reasons for the altered proliferation effects, we observed that CDK5 phosphorylates S308 on the androgen receptor (AR), resulting in its stabilization and differential expression of AR target genes including several growth-priming transcription factors. However, the amplified cell growth was found to be separated from AR signaling, further corroborated by CDK5-depdent proliferation of AR null cells. Instead, we found that the key growth-promoting effect was due to specific CDK5-mediated AKT activation. Down-regulation of CDK5 repressed AKT phosphorylation by altering its intracellular localization, immediately followed by prominent cell cycle inhibition. Taken together, these results suggest that CDK5 acts as a crucial signaling hub in prostate cancer cells by controlling androgen responses through AR, maintaining and accelerating cell proliferation through AKT activation, and releasing cell cycle breaks.


The Prostate ◽  
2008 ◽  
Vol 68 (9) ◽  
pp. 965-974 ◽  
Author(s):  
Claudio Festuccia ◽  
Giovanni Luca Gravina ◽  
Paola Muzi ◽  
Danilo Millimaggi ◽  
Vincenza Dolo ◽  
...  

The Prostate ◽  
2014 ◽  
Vol 74 (9) ◽  
pp. 946-958 ◽  
Author(s):  
Pengliang Shen ◽  
Jiabin Sun ◽  
Guiqin Xu ◽  
Li Zhang ◽  
Zhaojuan Yang ◽  
...  

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