Authors
Cellurale, Cristina ArrigoWeston, Claire R.
Reilly, Judith
Garlick, David S.
Jerry, D. Joseph
Sluss, Hayla Karen
Davis, Roger J.
UMass Chan Affiliations
Department of Medicine, Division of Endocrinology and MetabolismDepartment of Cancer Biology
Program in Molecular Medicine
Document Type
Journal ArticlePublication Date
2010-08-30Keywords
AnimalsBreast 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
Cancer Biology
Life Sciences
Medicine and Health Sciences
Neoplasms
Metadata
Show full item recordAbstract
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.Source
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 siteDOI
10.1371/journal.pone.0012469Permanent Link to this Item
http://hdl.handle.net/20.500.14038/39569PubMed ID
20814571Related Resources
Link to Article in PubMedRights
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.ae974a485f413a2113503eed53cd6c53
10.1371/journal.pone.0012469