MYCN amplification and overexpression are common in neuroendocrine prostate cancer (NEPC). However, the impact of aberrant N-Myc expression in prostate tumorigenesis and the cellular origin of NEPC have not been established. We define N-Myc and activated AKT1 as oncogenic components sufficient to transform human prostate epithelial cells to prostate adenocarcinoma and NEPC including the small cell prostate carcinoma (SCPC) variant with phenotypic and molecular features of aggressive, late-stage human disease. We directly show that prostate adenocarcinoma and NEPC can both arise from a common epithelial clone. Further, N-Myc is required for tumor maintenance and destabilization of N-Myc through Aurora A kinase inhibition reduces tumor burden. Our findings establish N-Myc as a driver of NEPC and a target for therapeutic intervention.;	Expression profiling by high throughput sequencing of experimentally generated human tumors with mixed NEPC and prostate adenocarcinoma. SOURCE: John LeeLaboratory of Owen Witte UCLA

GSE77624: Expression profiling by high throughput sequencing of tumors derived from human prostate epithelial cells transformed with the oncogenes N-Myc and myrAKT1.

Pluto Bioinformatics

GSE77624: Expression profiling by high throughput sequencing of tumors derived from human prostate epithelial cells transformed with the oncogenes N-Myc and myrAKT1.