PLX274568

GSE74798: Tumor-Specific Retrogene NANOGP8 Reprograms Prostate Cancer Cells to Castration Resistance by Engaging the FOXA1/AR Signaling Axis and MYC [RNA-seq]

• Organsim human
• Type RNASEQ
• Target gene
• Project ARCHS4

Targeted disruption of the embryonic stem cell (ESC) self-renewal and pluripotency factor NANOG diminishes cancer cell clonogenic growth in vitro and tumor development in vivo. NANOG has also been shown to augment CSC properties and propel the emergence of castration-resistance prostate cancer (CRPC) phenotypes. Here, we investigate the molecular mechanisms underlying NANOG-mediated oncogenesis and prostate cancer progression to androgen independence. ChIP-Seq analysis of LNCaP prostate cancer cells overexpressing doxycycline-inducible NANOG (either NANOG1 or NANOGP8 vs pLVX control) reveal that NANOG coordinately occupies regions of chromatin regulated by AR signaling steroid-receptor complex proteins AR, FOXA1 and NKX3.1. Taken together with the NANOG-induced changes in the prostate cancer transcriptome (RNA-Seq), NANOG appears to reprogram prostate cancer cells to castration resistance by converging on steroid-hormone receptor signaling. SOURCE: Collene Jeter (cjeter@mdanderson.org) - The University of Texas MD Anderson Cancer Center