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Pyrvinium pamoate targets to multiple vulnerabilities of Merkel cell carcinoma

ABSTRACT: Pyrvinium pamoate targets to multiple vulnerabilities of Merkel cell carcinoma

PROVIDER: PRJNA955382 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24174647_1.fastq.gz	Fastqsanger.gz
	SRR24174647_2.fastq.gz	Fastqsanger.gz
	SRR24174648_1.fastq.gz	Fastqsanger.gz
	SRR24174648_2.fastq.gz	Fastqsanger.gz
	SRR24174649_1.fastq.gz	Fastqsanger.gz

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Pyrvinium pamoate targets to multiple vulnerabilities of Merkel cell carcinoma

Project description:Among several WNT signaling perturbagens, we identified pyrvinium pamoate, an FDA-approved anthelminthic drug that exhibits anti-tumor abilities in multiple cancers. Through the integration of transcriptomic, network, and molecular analyses, we discovered that pyrvinium is broadly effective against Merkel cell carcinoma cell lines, and it targets multiple proposed MCC tumorigenesis pathways. Our study revealed that pyrvinium exerts anti-tumor activity in MCC not only through perturbing the canonical and non-canonical WNT signaling pathway but also non-specifically inhibiting cell growth - via the activation of the p53-mediated apoptosis pathway, modulation of mitochondrial function, and induction of endoplasmic reticulum (ER) stress.

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Project description:Pyrvinium pamoate, an anthelmintic drug, inhibits mitochondrial biogenesis during initial T-cell activation; however, its molecular target(s) and mechanism of action are unknown. In this study, we treated Jurkat T cell lysate with pyrvinium pamoate (5 nM and 50μM) and used proteome integral solubility alteration (PISA), to identify potential targets.

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Project description:Purpose: To compared Pyrvinium Pamoate induced transcription changes with known mitochondrial inhibitors. Methods: MIA-PaCa2 cells were treated with Pyrvinium Pamoate at 0.3µM, Oligomycin at 4µM or rotenone at 0.5 µM for 48 hours and then RNA was collected.

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Project description:To identify molecular effects of a classical anthelmintic pyrvinium pamoate(PP), we applied gene expression profiling in human acute leukemic cell line FLT3-ITD+ Molm13 using Whole Transcriptome Shotgun Sequencing (RNA-seq) after 6 h treatment with 50nM or 100nM pyrvinium. We got 94 and 219 differentially expressed genes (DEGs) compared with the control group, respectively. Among 94 DEGs in the 50nM pyrvinium group, 62 were upregulated and 32 were downregulated and corresponded 162 upregulated and 57 downregulated DEGs in the 100nM pyrvinium group.

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The antihelmintic drug pyrvinium pamoate targets aggressive breast cancer.

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Mouse Models of Pediatric Acute Megakaryoblastic Leukemia Reveal Novel Therapeutic Vulnerabilities [DSP750]

Project description:Pediatric acute megakaryoblastic leukemia (AMKL) is an aggressive blood cancer associated with poor therapeutic response and high mortality. We developed CBFA2T3-GLIS2-driven mouse models of AMKL that recapitulate the phenotypic and transcriptional signatures of the human disease. We show that CBFA2T3-GLIS2 and GLIS2 modulate similar transcriptional networks. Oncogenic RAS cooperates with GLIS2 to trigger AMKL, enhancing the penetrance and decreasing the latency of CBFA2T3-GLIS2-dependent AMKL. We find that the FDA-approved drug pyrvinium pamoate, a GLI protein inhibitor, can be repurposed to impair CBFA2T3-GLIS2 levels and promote AMKL cell death. In addition, consistent with our findings that both CBFA2T3-GLIS2 and GLIS2 alter the expression of numerous BH3-only proteins, murine and patient-derived AMKL cells are sensitive to the BCL-2 inhibitor navitoclax. We observe a striking synergistic response to combined treatment with pyrvinium pamoate and navitoclax, suggesting a novel therapeutic option for pediatric patients suffering from CBFA2T3-GLIS2-driven AMKL.

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