Abstract
Abstract The oncogenes PIM1 and c-MYC are frequently up-regulated in human prostate tumors. We found that PIM1 and c-MYC were co-expressed in human prostate cancer and were associated with higher Gleason scores. We next used a model of prostate regeneration coupled with lentiviral-mediated gene transfer to directly show that Pim1 dramatically enhanced c-MYC tumorigenicity in naïve adult mouse prostatic epithelium in a kinase-dependent manner. Microarray analysis revealed that many signaling pathways including MAPK, focal adhesion calcium signaling pathway were activated in MYC/Pim1 tumor. Knockdown of Pim1 in MYC/Pim1 tumor derived cell line reduced ERK and Akt phosphorylation. We further showed that targeting Pim1 by shRNA inhibited tumorigenicity in vitro and in vivo. Pim1 kinase inhibitor quercetagetin also inhibited cell growth in vitro. These results directly demonstrate that MYC and PIM1 cooperate in promoting tumor development. PIM1 can be considered as a drug target for human prostate cancer treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3239.
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