S 2-24: A Protein Kinase C Superfamily Member Mediates Invasive Prostate Cell Growth Downstream of Activated Phosphatidylinositol 3- Kinase
Posted on: Tuesday, 8 June 2004, 06:00 CDT
Conventional approaches to identify cancer targets are hampered by the chromosomal instability of tumor cells and often result in hundreds of differentially expressed genes with uncertain disease relevance. Instead of comparing disease endpoints we investigated the molecular changes induced after simulated loss of tumor suppressor function.
The tumor suppressor PTEN is required for the controlled and transient activation of the PI 3-kinase pathway that regulates a variety of cell responses. Loss of PTEN function results in increased invasive tumor cell growth caused by chronic activation of Pl 3-kinase signaling. To identify molecules that mediate malignant growth downstream of PI 3-kinase we used transient or inducible gene silencing and expression tools, which allowed us to compare pairs of otherwise isogenic cells. This approach was combined with expression profiling of cells grown in 3D cultures, which reflect the malignant potential of tumor cells more realistically than standard plastic culture conditions.
We present a protein kinase C-related molecule as novel mediator of invasive growth. This kinase is required for metastatic prostate cell growth as assessed by cell-based assays and in an orthotopic mouse tumor model. The protein is regulated by PI 3-kinase at multiple levels and might represent a target for therapeutic intervention in cancers lacking PTEN.
F. Leenders, K. Moepert, A. Santez, F. Czauderna, S. Dames, M. Aleku, M. Slernberger, S. Penschuk, A. Schmiedeknecht, T. Roehl, A. Wellmann, W. Arnold, K. W. Giese, J. Kaufmann and A. Kuppel.
atugen AG, Robert Roessle Str. 10, 13125 Berlin, Germany
Copyright Urban & Fischer Verlag Mar 2004
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