NDLI: Cooperativity of Nkx3.1 and Pten loss of function in a mouse model of prostate carcinogenesis.

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Cooperativity of Nkx3.1 and Pten loss of function in a mouse model of prostate carcinogenesis.

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Cooperativity of Nkx3.1 and Pten loss of function in a mouse model of prostate carcinogenesis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Abate-shen, C. Parsons, Ramon Cardiff, Robert D. Desai, Nishita Banach-petrosky, Whitney A. Kim, Minjung J. Shen, Michael M.
Description	Author Affiliation: Kim MJ ( Center for Advanced Biotechnology and Medicine and Department of Neuroscience, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.);
Abstract	Mouse models have provided significant insights into the molecular mechanisms of tumor suppressor gene function. Here we use mouse models of prostate carcinogenesis to demonstrate that the Nkx3.1 homeobox gene undergoes epigenetic inactivation through loss of protein expression. Loss of function of Nkx3.1 in mice cooperates with loss of function of the Pten tumor suppressor gene in cancer progression. This cooperativity results in the synergistic activation of Akt (protein kinase B), a key modulator of cell growth and survival. Our findings underscore the significance of interactions between tissue-specific regulators such as Nkx3.1 and broad-spectrum tumor suppressors such as Pten in contributing to the distinct phenotypes of different cancers.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	5
Volume Number	99
Language	English
Publisher	National Academy of Sciences
Publisher Date	2002-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Genes, Tumor Suppressor Homeodomain Proteins Physiology Phosphoric Monoester Hydrolases Prostatic Intraepithelial Neoplasia Pathology Prostatic Neoplasms Protein-Serine-Threonine Kinases Transcription Factors Tumor Suppressor Proteins Alleles Animals Disease Models, Animal Disease Progression Enzyme Activation Gene Expression Genetics Metabolism Loss Of Heterozygosity Mice Mice, Inbred C57BL Mice, Knockout PTEN Phosphohydrolase Proto-Oncogene Proteins Proto-Oncogene Proteins C-akt Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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