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Targets of c-Jun NH₂-terminal Kinase 2-mediated Tumor Growth Regulation Revealed by Serial Analysis of Gene Expression

Cell Stress and Aging Section, Laboratory of Cellular and Molecular Biology [O. P., M. G., R. H. D., N. J. H.] and Molecular Cardiology Unit, Laboratory of Cardiovascular Science [S. V. A., K. R. B.], Gerontology Research Center, National Institute on Aging-IRP, Baltimore, Maryland 21224, and Isis Pharmaceuticals, Inc., Carlsbad, California 92008 [W. A. G.]

Although the c-Jun NH₂-terminal kinase (JNK) pathway has been implicated in mediating cell growth and transformation, its downstream effectors remain to be identified. Using JNK2 antisense oligonucleotides (JNK2AS), we uncovered previously a role for JNK2 in regulating cell cycle progression and survival of human PC3 prostate carcinoma cells. Here, to identify genes involved in implementing JNK2-mediated effects, we have analyzed global gene expression changes in JNK2-deprived PC3 cells using Serial Analysis of Gene Expression. More than 40,000 tags each were generated from control and PC3-JNK2AS libraries, corresponding to 15,999 and 20,698 unique transcripts, respectively. Transcripts corresponding to transcription factors, stress-induced genes, and apoptosis-related genes were up-regulated in the PC3-JNK2AS library, revealing a significant stress response after the inhibition of JNK2 expression. Genes involved in DNA repair, mRNA turnover, and drug resistance were found to be down-regulated by inhibition of JNK2 expression, further highlighting the importance of JNK2 signaling in regulating cell homeostasis and tumor cell growth.

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