PubMed ID
20814571
UMMS Affiliation
Program in Molecular Medicine; Department of Cancer Biology; Department of Medicine, Division of Endocrinology and Metabolism
Date
8-30-2010
Document Type
Article
Subjects
Animals; Breast Neoplasms; Disease Models, Animal; Female; Mammary Glands, Animal; Mice; Mice, Inbred BALB C; Mitogen-Activated Protein Kinase 8; Mitogen-Activated Protein Kinase 9; Survival Analysis; Tumor Suppressor Protein p53
Disciplines
Cancer Biology | Life Sciences | Medicine and Health Sciences | Neoplasms
Abstract
The cJun NH2-terminal kinase (JNK) signal transduction pathway has been implicated in mammary carcinogenesis. To test the role of JNK, we examined the effect of ablation of the Jnk1 and Jnk2 genes in a Trp53-dependent model of breast cancer using BALB/c mice. We detected no defects in mammary gland development in virgin mice or during lactation and involution in control studies of Jnk1(-/-) and Jnk2(-/-) mice. In a Trp53(-/+) genetic background, mammary carcinomas were detected in 43% of control mice, 70% of Jnk1(-/-) mice, and 53% of Jnk2(-/-) mice. These data indicate that JNK1 and JNK2 are not essential for mammary carcinoma development in the Trp53(-/+) BALB/c model of breast cancer. In contrast, this analysis suggests that JNK may partially contribute to tumor suppression. This conclusion is consistent with the finding that tumor-free survival of JNK-deficient Trp53(-/+) mice was significantly reduced compared with control Trp53(-/+) mice. We conclude that JNK1 and JNK2 can act as suppressors of mammary tumor development.
Comments
Citation: Cellurale C, Weston CR, Reilly J, Garlick DS, Jerry DJ, et al. (2010) Role of JNK in a Trp53-Dependent Mouse Model of Breast Cancer. PLoS ONE 5(8): e12469. doi:10.1371/journal.pone.0012469. Link to article on publisher's site
Copyright: © 2010 Cellurale et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.