Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 106, Issue 31, Pages 12962-12967Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0813055106
Keywords
AKT; aPKC; IL-6; inflammation; prostate cancer
Categories
Funding
- University of Cincinnati-Consejo Superior de Investigaciones Cientificas Research Collaborative Agreement
- National Institutes of Health [R01-AI072581]
- Spanish National Cancer Research Center
- Spanish Ministry of Education
- European Union
- Marcelino Botin'' Foundation
- Instituto de Salud Carlos III/FIS and Fundacion Progreso y Salud
- Consejeria de Salud Junta de Andalucia
Ask authors/readers for more resources
Prostate cancer is one of the most common neoplasias in men. The tumor suppressor Par-4 is an important negative regulator of the canonical NF-kappa B pathway and is highly expressed in prostate. Here we show that Par-4 expression is lost in a high percentage of human prostate carcinomas, and this occurs in association with phosphatase and tensin homolog deleted from chromosome 10 ( PTEN) loss. Par-4 null mice, similar to PTEN-heterozygous mice, only develop benign prostate lesions, but, importantly, concomitant Par-4 ablation and PTEN-heterozygosity lead to invasive prostate carcinoma in mice. This strong tumorigenic cooperation is anticipated in the preneoplastic prostate epithelium by an additive increase in Akt activation and a synergistic stimulation of NF-kappa B. These results establish the cooperation between Par-4 and PTEN as relevant for the development of prostate cancer and implicate the NF-kappa B pathway as a critical event in prostate tumorigenesis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available