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Tumor-Specific Retrogene NANOGP8 Reprograms Prostate Cancer Cells to Castration Resistance by Engaging the FOXA1/AR Signaling Axis and MYC

ABSTRACT: Tumor-Specific Retrogene NANOGP8 Reprograms Prostate Cancer Cells to Castration Resistance by Engaging the FOXA1/AR Signaling Axis and MYC

PROVIDER: PRJNA301560 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2930940.fastq.gz	Fastqsanger.gz
	SRR2930950_1.fastq.gz	Fastqsanger.gz
	SRR2930950_2.fastq.gz	Fastqsanger.gz
	SRR2930960_1.fastq.gz	Fastqsanger.gz
	SRR2930960_2.fastq.gz	Fastqsanger.gz

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

Project description: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.

2016-11-08 | GSE74798 | GEO

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

Project description:Targeted disruption of the embryonic stem cell (ESC) self-renewal and pluripotency factor NANOG has been shown to diminish 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.

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NANOG reprograms prostate cancer cells to castration resistance via dynamically repressing and engaging the AR/FOXA1 signaling axis.

Project description:The pluripotency transcription factor NANOG has been implicated in tumor development, and NANOG-expressing cancer cells manifest stem cell properties that sustain tumor homeostasis, mediate therapy resistance and fuel tumor progression. However, how NANOG converges on somatic circuitry to trigger oncogenic reprogramming remains obscure. We previously reported that inducible NANOG expression propels the emergence of aggressive castration-resistant prostate cancer phenotypes. Here we first show that endogenous NANOG is required for the growth of castration-resistant prostate cancer xenografts. Genome-wide chromatin immunoprecipitation sequencing coupled with biochemical assays unexpectedly reveals that NANOG co-occupies a distinctive proportion of androgen receptor/Forkhead box A1 genomic loci and physically interacts with androgen receptor and Forkhead box A1. Integrative analysis of chromatin immunoprecipitation sequencing and time-resolved RNA sequencing demonstrates that NANOG dynamically alters androgen receptor/Forkhead box A1 signaling leading to both repression of androgen receptor-regulated pro-differentiation genes and induction of genes associated with cell cycle, stem cells, cell motility and castration resistance. Our studies reveal global molecular mechanisms whereby NANOG reprograms prostate cancer cells to a clinically relevant castration-resistant stem cell-like state driven by distinct NANOG-regulated gene clusters that correlate with patient survival. Thus, reprogramming factors such as NANOG may converge on and alter lineage-specific master transcription factors broadly in somatic cancers, thereby facilitating malignant disease progression and providing a novel route for therapeutic resistance.

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

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Homo sapiens

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

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Tumor-Specific Retrogene NANOGP8 Reprograms Prostate Cancer Cells to Castration Resistance by Engaging the FOXA1/AR Signaling Axis and MYC

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