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      Identification of the JNK signaling pathway as a functional target of the tumor suppressor PTEN.

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          Abstract

          Although most oncogenic phenotypes of PTEN loss are attributed to AKT activation, AKT alone is not sufficient to induce all of the biological activities associated with PTEN inactivation. We searched for additional PTEN-regulated pathways through gene set enrichment analysis (GSEA) and identified genes associated with JNK activation. PTEN null cells exhibit higher JNK activity, and genetic studies demonstrate that JNK functions parallel to and independently of AKT. Furthermore, PTEN deficiency sensitizes cells to JNK inhibition and negative feedback regulation of PI3K was impaired in PTEN null cells. Akt and JNK activation are highly correlated in human prostate cancer. These findings implicate JNK in PI3K-driven cancers and demonstrate the utility of GSEA to identify functional pathways using genetically defined systems.

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          Author and article information

          Journal
          Cancer Cell
          Cancer cell
          Elsevier BV
          1535-6108
          1535-6108
          Jun 2007
          : 11
          : 6
          Affiliations
          [1 ] Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA 90095, USA.
          Article
          S1535-6108(07)00146-8
          10.1016/j.ccr.2007.04.021
          17560336
          3606c263-151e-4802-bb84-0c3b783458d0
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