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Opioid agonists as potential AML therapy

ABSTRACT: Opioid agonists as potential AML therapy

PROVIDER: PRJNA615085 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11413511_1.fastq.gz	Fastqsanger.gz
	SRR11413511_2.fastq.gz	Fastqsanger.gz
	SRR11413512_1.fastq.gz	Fastqsanger.gz
	SRR11413512_2.fastq.gz	Fastqsanger.gz
	SRR11413513_1.fastq.gz	Fastqsanger.gz

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Opioid agonists as potential AML therapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-20 | GSE147511 | GEO

Opioid receptor signaling suppresses leukemia by inducing TET-dependent DNA demethylation

Project description:Acute myeloid leukemia (AML) is a type of heterogeneous and fatal hematopoietic malignancy. The ten-eleven translocation (TET) mediated DNA demethylation is known to be critically associated with AML pathogenesis. Through chemical compound screening, we found that the opioid receptor agonist, loperamide hydrochloride (OPA1), significantly suppresses AML cell viability. The potential therapeutic effects of opioid receptor agonists, especially OPA1, were then verified in AML cells in vitro, and t(11q23) and t(8;21) AML mouse models in vivo. OPA1-induced activation of OPRM1 enhanced the transcription of TET2, increased DNA 5-hydroxymethylcytosine (5hmC) modification, and in turn, activated NFκB signaling. Notably, AML with TET2 mutations or chemotherapy resistance were highly sensitive to OPA1. Our results reveal a previously unknown OPRM1-TET2-5hmC-TRAF2 regulatory axis in AML, and suggest that opioid agonists, particularly OPA1, an FDA-approved antidiarrheal drug, have therapeutic potential in AML, especially in TET2 mutated and chemotherapy-resistant AML, which have a poor prognosis.

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Opioid receptor signaling suppresses leukemia by inducing TET-dependent DNA demethylation [RNA-seq]

Project description:Acute myeloid leukemia (AML) is a group of heterogeneous diseases with high malignancy. The ten-eleven translocation (TET) mediated DNA demethylation was known to be critically associated with AML pathogenesis. Through chemical compound screening, we found an opioid receptor agonist, namely loperamide hydrochloride (OPA1), most significantly suppressed AML cell viability. The potential therapeutic effects of opioid receptor agonists, especially OPA1, were then verified in AML cells in vitro, and AML mouse models carrying t(11q23) and t(8;21) in vivo. OPA1-induced activation of OPRM1 enhanced the transcription of TET2, increased DNA 5-hydroxymethylcytosine (5hmC) modification, and in turn, activated NFκB signaling. Notably, AML with TET2 mutations or chemotherapy resistance were sensitive to OPA1. Our results unveiled the previously unappreciated OPRM1-TET2-5hmC-TRAF2 regulatory axis in AML, and highlighted the therapeutic potential of opioid agonists, particularly OPA1, a FDA-approved antidiarrheal drug, in treating AML, especially TET2 mutated AML and chemotherapy-resistant AML, which were known to have poor prognosis.

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Opioid receptor signaling suppresses leukemia by inducing TET-dependent DNA demethylation [5hmC-seq]

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Opioid receptor signaling suppresses leukemia by inducing TET-dependent DNA demethylation [ChIP-seq]

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Effect of peripheral kappa-opioid receptor agonists on murine T cells

Project description:This study investigated the transcriptional responses of murine T cell subsets to treatment with novel peripherally restricted, perhydroquinoxaline-derived kappa opioid receptor (KOR) agonists. We sorted and polarized primary murine CD4+ and CD8+ T cells towards Th1, Th17, Treg and CD8+ T cells and stimulated them with novel KOR agonists or vehicle control (DMSO). RNA sequencing was performed to assess gene expression changes associated with KOR activation across distinct T cell subsets.

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Effect of peripheral kappa-opioid receptor agonists on murine T cells

Project description:Effect of peripheral kappa-opioid receptor agonists on murine T cells

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Genomics of therapy Related MDS and AML

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Genomics of therapy Related MDS and AML

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Agonist-selective NOP receptor phosphorylation correlates in vitro and in vivo and reveals differential post-activation signaling by chemically diverse agonists

Project description:Agonists for the nociceptin/orphanin FQ opioid peptide NOP receptor, a member of the opioid receptor family, are under active investigation as novel analgesics, but their modes of signaling are less well characterized than those for other members of the opioid receptor family. Therefore, we investigated whether different NOP receptor ligands show differential signaling or functional selectivity at the NOP receptor. Using newly developed phosphosite-specific antibodies to NOP receptor, we found that agonist-induced NOP receptor phosphorylation occurred primarily at four carboxyl-terminal serine (S) and threonine (T) residues, namely Ser346, Ser351, Thr362 and Ser363, and proceeded with a temporal hierarchy, with Ser346 as the first site of phosphorylation. G protein-coupled receptor kinases 2 and 3 (GRK2/3) cooperated during agonist-induced phosphorylation, which in turn facilitated NOP receptor desensitization and internalization. A comparison of structurally distinct NOP receptor agonists revealed dissociation in functional efficacies between G protein-dependent signaling and receptor phosphorylation. Furthermore, in vivo, in NOP-eGFP and NOP-eYFP mice, NOP receptor agonists induced multisite phosphorylation and internalization in a dose-dependent and agonist-selective manner that could be blocked by specific antagonists. Together, our study provides novel tools to study ligand-activated NOP receptor signaling in vitro and in vivo. Differential agonist-selective NOP receptor phosphorylation by chemically diverse NOP receptor agonists suggests that differential signaling by NOP receptor agonists may play a role in NOP receptor ligand pharmacology.

2020-05-26 | PXD012908 | Pride

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