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High-throughput Drug Screening Identifies Ketotifen as a Potential Therapeutic Agent for Neuroendocrine Prostate Cancer

ABSTRACT: High-throughput Drug Screening Identifies Ketotifen as a Potential Therapeutic Agent for Neuroendocrine Prostate Cancer

PROVIDER: PRJNA933562 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23393600_1.fastq.gz	Fastqsanger.gz
	SRR23393600_2.fastq.gz	Fastqsanger.gz
	SRR23393597_1.fastq.gz	Fastqsanger.gz
	SRR23393597_2.fastq.gz	Fastqsanger.gz
	SRR23393598_1.fastq.gz	Fastqsanger.gz

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Project description:Here, we performed a high-throughput drug screening and identified fluoxetine, originally an FDA-approved antidepressant, as candidate therapeutic agent for NEPC. In vitro experiments revealed that fluoxetine effectively curbed the neuroendocrine differentiation and inhibited the cell viability by targeting the AKT pathway. Altogether, this work repurposed fluoxetine for antitumor application, and supported its clinical development for NEPC therapy, which may provide a promising therapeutic strategy.

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High-throughput Drug Screening Identifies Ketotifen as a Potential Therapeutic Agent for Neuroendocrine Prostate Cancer

Project description:We performed a high-throughput drug screening and identified Ketotifen, originally an FDA-approved antidepressant, as candidate therapeutic agent for NEPC. RNA-seq was performed of LASCPC-01 cells treated with Ketotifen or PBS.

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High-throughput Drug Screening Identifies Fluoxetine as a Potential Therapeutic Agent for Neuroendocrine Prostate Cancer

Project description:High-throughput Drug Screening Identifies Fluoxetine as a Potential Therapeutic Agent for Neuroendocrine Prostate Cancer

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High-throughput drug screening identifies fluoxetine as a potential therapeutic agent for neuroendocrine prostate cancer.

Project description:IntroductionNeuroendocrine prostate cancer (NEPC) is an aggressive subtype of prostate cancer with poor prognosis and resistance to hormone therapy, which has limited therapeutic approaches. Therefore, this study aimed to identify a novel treatment for NEPC and provide evidence of its inhibitory effects.MethodsWe performed a high-throughput drug screening and identified fluoxetine, originally an FDA-approved antidepressant, as candidate therapeutic agent for NEPC. We carried out both in vitro and in vivo experiments to demonstrate the inhibitory effects of fluoxetine on NEPC models and its mechanism in detail.ResultsOur results demonstrated that fluoxetine effectively curbed the neuroendocrine differentiation and inhibited cell viability by targeting the AKT pathway. Preclinical test in NEPC mice model (PBCre4: Ptenf/f; Trp53f/f; Rb1f/f) showed that fluoxetine effectively prolonged the overall survival and reduced the risk of tumor distant metastases.DiscussionThis work repurposed fluoxetine for antitumor application, and supported its clinical development for NEPC therapy, which may provide a promising therapeutic strategy.

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A Drug Repurposing Screen Identifies Fludarabine Phosphate as a Potential Therapeutic Agent for N-MYC Overexpressing Neuroendocrine Prostate Cancers

Project description:Neuroendocrine prostate cancer (NEPC) represents a highly aggressive form of prostate tumors. NEPC results from trans-differentiated castration-resistant prostate cancer (CRPC) with increasing evidence indicating that the incidence of NEPC often results from the adaptive response to androgen deprivation therapy. Recent studies have shown that a subset of NEPC exhibits overexpression of the MYCN oncogene along with the loss of tumor suppressing TP53 and RB1 activities. N-MYC is structurally disordered with no binding pockets available on its surface and so far, no clinically approved drug is available. We adopted a drug-repurposing strategy, screened ~1800 drug molecules and identified Fludarabine Phosphate to preferentially inhibit proliferation of N-MYC overexpressing NEPC cells by inducing ROS. We also show that Fludarabine phosphate affects N-MYC protein levels and N-MYC transcriptional targets in NEPC cells. Moreover, enhanced ROS production destabilizes N-MYC protein by inhibiting AKT signaling and is responsible for the reduced survival of NEPC cells and tumors. Our results indicate that increasing ROS production by administration of Fludarabine Phosphate may represent an effective treatment option for patients with N-MYC overexpressing NEPC tumors.

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