scholarly journals Nucleoporin 153 regulates estrogen-dependent nuclear translocation of endothelial nitric oxide synthase and estrogen receptor beta in prostate cancer

Oncotarget ◽  
2018 ◽  
Vol 9 (46) ◽  
pp. 27985-27997 ◽  
Author(s):  
Agnese Re ◽  
Claudia Colussi ◽  
Simona Nanni ◽  
Aurora Aiello ◽  
Lorenza Bacci ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Nitric Oxide ◽  
Estrogen Receptor ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Nuclear Translocation ◽  
Estrogen Receptor Beta ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Receptor Beta

The role of nuclear endothelial nitric oxide synthase in the endothelial and prostate microenvironments

2011 ◽  
Vol 5 (2) ◽  
Author(s):  
Simona Nanni ◽  
Annalisa Grasselli ◽  
Valentina Benvenuti ◽  
Aurora Aiello ◽  
Valentina Pantisano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Target Genes ◽  
Nuclear Translocation ◽  
Androgen Independence ◽  
Human Telomerase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

AbstractThis review is based on novel observations from our laboratory on the nuclear translocation and functional role of endothelial nitric oxide synthase (eNOS) in endothelial and prostate cancer (PCa) epithelial cells. Nitric oxide (NO), the product of eNOS, is a free radical involved in the physiology and pathophysiology of living organisms and in a variety of biological processes including the maintenance of vascular homeostasis. Of relevance in this context is the role that estrogens play in the apoptotic process and the migration of endothelial cells through the regulation of target genes such as eNOS itself. It has been shown that both estrogen and NO signaling, mediated respectively by the estrogen receptors (ERs) and eNOS, can strongly counteract endothelial senescence through a common effector, the catalytic subunit of human telomerase. Therefore, this protein has been identified as a key molecule in the aging process which, intriguingly, is considered the only risk factor in the development of PCa and one of the major determinants of cardiovascular diseases. Indeed, in both these contexts we have defined a molecular mechanism involving activation of eNOS and hypoxia-inducible factors in association with ERβ that characterizes the most aggressive form of PCa or influences endothelial cell differentiation. Altogether these data led us to postulate that activation of eNOS is a crucial requirement for the delaying of endothelial senescence as well as for the acquisition of androgen-independence and for tumor progression in the prostate microenvironment.

Sign in / Sign up

Export Citation Format

Share Document