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Neuropilin-2 Promotes the Development of Neuroendocrine Prostate Cancer

ABSTRACT: Neuropilin-2 Promotes the Development of Neuroendocrine Prostate Cancer

PROVIDER: PRJNA856296 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20005633_1.fastq.gz	Fastqsanger.gz
	SRR20005633_2.fastq.gz	Fastqsanger.gz
	SRR20005634_1.fastq.gz	Fastqsanger.gz
	SRR20005634_2.fastq.gz	Fastqsanger.gz

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Neuropilin-2 Promotes the Development of Neuroendocrine Prostate Cancer

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DPYSL5 is Highly Expressed in treatment-induced Neuroendocrine Prostate Cancer and Promotes Lineage Plasticity via EZH2/PRC2

Project description:Treatment-induced neuroendocrine prostate cancer (t-NEPC) is a lethal subtype of castration-resistant prostate cancer resistant to androgen receptor (AR) inhibitors. Our study unveils that AR suppresses neuronal development protein dihydropyrimidinase-related protein 5 (DPYSL5), providing a mechanism for neuroendocrine transformation under androgen deprivation therapy. Our unique CRPC-NEPC cohort with 157 patient samples, including 55 t-NEPC patient samples, shows a high expression of DPYSL5 in t-NEPC patients, and that DPYSL5 correlates with neuroendocrine markers and inversely with AR and PSA. DPYSL5 overexpression in prostate cancer cells induces neuron like phenotype, enhances invasion, proliferation, and upregulates stemness and neuroendocrine related markers. Mechanistically, DPYSL5 promotes prostate cancer cell plasticity via EZH2-mediated PRC2 activation. Depletion of DPYSL5 halts proliferation, induces G1 phase cell cycle arrest, reverses neuroendocrine phenotype and upregulates luminal genes. In conclusion, DPYSL5 plays a critical role in regulating prostate cancer cell plasticity, and we propose the AR/DPYSL5/EZH2/PRC2 axis as a novel driver of t-NEPC progression.

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Project description:Gene expression was first compared between prostate adenocarcinoma cell line LNCaP C4-2 and our developed neuroendocrine like derived cell line DKD (LNCaP C4-2 stably depleted with TP53 and RB1). In the next set, we compared the gene expression of neuroendocrine like DKD under presence and absence of Neurolipilin-2.

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Post-transcriptional gene regulation by microRNA-194 promotes neuroendocrine transdifferentiation in prostate cancer

Project description:Potent therapeutic inhibition of the androgen receptor (AR) in prostate adenocarcinoma can lead to the emergence of neuroendocrine prostate cancer (NEPC), a phenomenon associated with enhanced cell plasticity. Here, we show that microRNA-194 (miR-194) is a regulator of epithelial-neuroendocrine transdifferentiation. In clinical prostate cancer samples, miR-194 expression and activity were elevated in NEPC and inversely correlated with AR signalling. Over-expression of miR-194 facilitated the emergence of neuroendocrine features in prostate cancer cells, a process mediated by its ability to directly target a suite of genes involved in cell plasticity. One such target gene was FOXA1, which encodes a transcription factor with a vital role in maintaining the prostate epithelial lineage. Importantly, a miR-194 inhibitor blocked epithelial-neuroendocrine transdifferentiation and inhibited the growth of cell lines and patient-derived organoids possessing neuroendocrine features. Overall, our study reveals a post-transcriptional mechanism regulating the plasticity of prostate cancer cells and provides a rationale for targeting miR-194 in NEPC.

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Post-transcriptional gene regulation by microRNA-194 promotes neuroendocrine transdifferentiation in prostate cancer

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The placental gene PEG10 promotes progression of neuroendocrine prostate cancer

Project description:The placental gene PEG10 promotes progression of neuroendocrine prostate cancer

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Post-transcriptional gene regulation by microRNA-194 promotes neuroendocrine transdifferentiation in prostate cancer [ChIP-Seq]

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