UMMS Affiliation
Program in Molecular Medicine
Publication Date
2011-04-01
Document Type
Article
Subjects
Animals; Apoptosis; Cadherins; Cell Proliferation; Cell Transformation, Neoplastic; Contact Inhibition; Fibroblasts; JNK Mitogen-Activated Protein Kinases; Lung Neoplasms; Mice; Precancerous Conditions; Proto-Oncogene Proteins p21(ras); Signal Transduction; Stress, Physiological; Tumor Stem Cell Assay; Tumor Suppressor Protein p53
Disciplines
Biochemistry | Cancer Biology | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
Abstract
The c-Jun NH(2)-terminal kinase (JNK) signal transduction pathway causes increased gene expression mediated, in part, by members of the activating transcription factor protein (AP1) group. JNK is therefore implicated in the regulation of cell growth and cancer. To test the role of JNK in Ras-induced tumor formation, we examined the effect of compound ablation of the ubiquitously expressed genes Jnk1 plus Jnk2. We report that JNK is required for Ras-induced transformation of p53-deficient primary cells in vitro. Moreover, JNK is required for lung tumor development caused by mutational activation of the endogenous KRas gene in vivo. Together, these data establish that JNK plays a key role in Ras-induced tumorigenesis.
Rights and Permissions
The authors have paid a fee to allow immediate free access to this article. Publisher's author rights policy at http://journals.asm.org/site/misc/ASM_Author_Statement.xhtml also allows posting of publisher PDF.
DOI of Published Version
10.1128/MCB.01122-10
Source
Mol Cell Biol. 2011 Apr;31(7):1565-76. doi: 10.1128/MCB.01122-10. Epub 2011 Jan 31. Link to article on publisher's site
Journal/Book/Conference Title
Molecular and cellular biology
Related Resources
PubMed ID
21282468
Repository Citation
Cellurale, Cristina Arrigo; Sabio, Guadalupe; Kennedy, Norman J.; Das, Madhumita; Bylsma, Marissa; Sandy, Peter; Jacks, Tyler; and Davis, Roger J., "Requirement of c-Jun NH(2)-terminal kinase for Ras-initiated tumor formation" (2011). Davis Lab Publications. 31.
https://escholarship.umassmed.edu/davis/31
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Biochemistry Commons, Cancer Biology Commons, Cell Biology Commons, Cellular and Molecular Physiology Commons, Molecular Biology Commons