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[Cancer Research 62, 1343-1348, March 1, 2002]
© 2002 American Association for Cancer Research

Carcinogenesis

Deficiency of c-Jun-NH2-terminal Kinase-1 in Mice Enhances Skin Tumor Development by 12-O-Tetradecanoylphorbol-13-Acetate1

Qing-Bai She, Nanyue Chen, Ann M. Bode, Richard A. Flavell and Zigang Dong2

The Hormel Institute, University of Minnesota, Austin, Minnesota 55912 [Q-B. S., N. C., A. M. B., Z. D.], and Department and Section of Immunology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520 [R. A. F.]

The c-Jun NH2-terminal kinase (JNK) has been implicated in regulating cell survival, apoptosis, and transformation. However, the distinct role of JNK isoforms in regulating tumor development is not yet clear. We have found previously that skin tumor formation induced by the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), is suppressed in JNK2-deficient (Jnk2-/-) mice. Here, we show that JNK1-deficient (Jnk1-/-) mice are more susceptible to TPA-induced skin tumor development than wild-type mice. The rate of tumor development in Jnk1-/- mice was significantly more rapid than that observed in wild-type mice (P < 0.0001). At the end of 33 weeks of TPA promotion, the number of skin tumors and tumors >1.5 mm in diameter per mouse in Jnk1-/- mice was significantly increased by 71% (P < 0.03) and 82% (P < 0.03), respectively, relative to the wild-type mice. Furthermore, the carcinoma incidence and the number of carcinomas per mouse were also higher in Jnk1-/- mice. Strikingly, Jnk1-/- mouse skin was more sensitive to TPA-induced AP-1 DNA binding activity and phosphorylation of extracellular signal-regulated kinases and Akt, which are two important survival signaling components. These results suggest that JNK1 is a crucial suppressor of skin tumor development.




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Copyright © 2002 by the American Association for Cancer Research.