Program in Molecular Medicine
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
Biochemistry | Cancer Biology | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
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.
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DOI of Published Version
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
Molecular and cellular biology
Cellurale CA, Sabio G, Kennedy NJ, Das M, Bylsma M, Sandy P, Jacks T, Davis RJ. (2011). Requirement of c-Jun NH(2)-terminal kinase for Ras-initiated tumor formation. Davis Lab Publications. https://doi.org/10.1128/MCB.01122-10. Retrieved from https://escholarship.umassmed.edu/davis/31