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Pharmacologic activation of G protein-coupled estrogen receptor inhibits pancreatic ductal adenocarcinoma

ABSTRACT: Pharmacologic activation of G protein-coupled estrogen receptor inhibits pancreatic ductal adenocarcinoma

PROVIDER: PRJNA481745 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7537070.fastq.gz	Fastqsanger.gz
	SRR7537080.fastq.gz	Fastqsanger.gz
	SRR7537071.fastq.gz	Fastqsanger.gz
	SRR7537081.fastq.gz	Fastqsanger.gz
	SRR7537072.fastq.gz	Fastqsanger.gz

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Pharmacologic activation of G protein-coupled estrogen receptor inhibits pancreatic ductal adenocarcinoma

Project description:We examine the effect of GPER activation on murine pancreatic ductal adenocarcinoma cell lines

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Pharmacologic Activation of the G Protein-Coupled Estrogen Receptor Inhibits Pancreatic Ductal Adenocarcinoma.

Project description:Background & aimsFemale sex is associated with lower incidence and improved clinical outcomes for most cancer types including pancreatic ductal adenocarcinoma (PDAC). The mechanistic basis for this sex difference is unknown. We hypothesized that estrogen signaling may be responsible, despite the fact that PDAC lacks classic nuclear estrogen receptors.MethodsHere we used murine syngeneic tumor models and human xenografts to determine that signaling through the nonclassic estrogen receptor G protein-coupled estrogen receptor (GPER) on tumor cells inhibits PDAC.ResultsActivation of GPER with the specific, small molecule, synthetic agonist G-1 inhibited PDAC proliferation, depleted c-Myc and programmed death ligand 1 (PD-L1), and increased tumor cell immunogenicity. Systemically administered G-1 was well-tolerated in PDAC bearing mice, induced tumor regression, significantly prolonged survival, and markedly increased the efficacy of PD-1 targeted immune therapy. We detected GPER protein in a majority of spontaneous human PDAC tumors, independent of tumor stage.ConclusionsThese data, coupled with the wide tissue distribution of GPER and our previous work showing that G-1 inhibits melanoma, suggest that GPER agonists may be useful against a range of cancers that are not classically considered sex hormone responsive and that arise in tissues outside of the reproductive system.

| S-EPMC7578406 | biostudies-literature

Profile of estrogen-responsive genes in an estrogen-specific mammary gland outgrowth model

Project description:Both ovarian and pituitary hormones are required for the pubertal development of the mouse mammary gland. Estradiol directs ductal elongation and branching within the adipose stroma of the adolescent mouse mammary gland, while progesterone leads to tertiary branching and alveolar development. The purpose of this investigation was to identify the estrogen-responsive genes that are associated with estrogen-stimulated ductal elongation and branching in the mouse mammary gland in the absence of other ovarian hormones. We also wanted to determine if estrogen-responsive gene regulation at early stages of ductal elongation (ie. when ductal growth was minimal) was similar to those regulated after significant ductal elongation had occurred. To identify estrogen-regulated genes, ovariectomized prepubertal mice were exposed to 17beta-estradiol for four weeks, and mammary gland global gene expression analyzed by microarray analysis at various points during this time course. We determined that while many genes are regulated in all weeks of treatment, there remained a subset of genes that was uniquely regulated at each time-point. This observation was reflected in the biological functions of these genes; some categories were represented in all weeks of treatment while others were specific to only certain time-points. We have also identified estradiol-responsive genes in the mouse mammary gland that co-express with Estrogen Receptor alpha in human breast cancer, which may represent novel effectors of estrogen action and/or biomarkers for the progression of estrogen-dependent cancers and other estrogen-driven diseases.

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Estrogen Promotes Mandibular Condylar Fibrocartilage Chondrogenesis and Inhibits Degeneration Via Estrogen Receptor Alpha in Female Mice

Project description:Estrogen Promotes Mandibular Condylar Fibrocartilage Chondrogenesis and Inhibits Degeneration Via Estrogen Receptor Alpha in Female Mice

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Therapeutic Activation of G Protein-Coupled Estrogen Receptor 1 in Waldenström Macroglobulinemia

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Estrogen receptor α-mediated signaling inhibits type I interferon response to promote breast cancer

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Nuclear Estrogen Receptor alpha (ERα) interactome following estrogen and antiestrogen treatment.

Project description:The Estrogen Receptor alpha (ERα) controls key cellular functions in hormone responsive breast cancer by assembling in large functional multiprotein complexes. ERα ligands are classified as agonists and antagonist, according to the response they elicit, thus the molecular characterization of the of ERα nuclear iteractome composition following estrogen and antiestrogen stimulation whose is needed to understand their effects on estrogen target tissues, in particular breast cancer. To this aim interaction proteomics coupled to mass spectrometry (MS) was applied to map the ERα nuclear interacting partners in MCF7 breast cancer cell nuclei following estrogen and antiestrogen stimuli.

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Estrogen inhibits the progression of liver cancer by modulating PRDX-induced ferroptosis

Project description:Liver cancer exhibits significant gender disparities, with men having a 2-5 times higher risk of developing liver cancer compared to women. Numerous studies have demonstrated the influence of estrogen on liver cancer development, although the precise underlying mechanism remains unclear. Peroxiredoxins (PRDXs) represent a recently identified peroxidase family that modulates various signaling pathways associated with reactive oxygen species. This research aims to explore the impact of estrogen on the expression of PRDX1, PRDX5, and PRDX6 in hepatocellular carcinoma cells, thereby modulating liver cancer progression. Treatment with estrogen and the silencing of PRDX1, PRDX5, and PRDX6 impairs the proliferative capacity of hepatocarcinoma cells. The levels of PRDX1, PRDX5, and PRDX6 were found to be elevated in hepatocellular carcinoma compared to normal tissues, with estrogen demonstrating the ability to decrease their expression in hepatocellular carcinoma cells. Furthermore, estrogen influences the expression of PRDXs (PRDX5 and PRDX6) by regulating RASA1. Additionally, estrogen stimulation impacts ferroptosis in hepatocellular carcinoma cells, suggesting that PRDXs and ferroptosis-related genes are estrogen-responsive genes that promote liver cancer progression. Elevated LPCAT3 levels and downregulation of PRDX1, PRDX5, and PRDX6 expression may potentially manage the advancement of HCC.

2024-08-26 | PXD055317 |

Estrogen Receptor β Activation Inhibits Colitis by Promoting the NLRP6-Mediated Autophagy

Project description:Estrogen Receptor β Activation Inhibits Colitis by Promoting the NLRP6-Mediated Autophagy

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Therapeutic Activation of G Protein-Coupled Estrogen Receptor 1 in Waldenström Macroglobulinemia

Project description:Activation of G protein-coupled estrogen receptor 1 (GPER1) is an attractive therapeutic strategy to treat a variety of human diseases, including cancer. Here, we show that GPER1 is remarkably upregulated in tumor cells derived from different cohorts of Waldenström Macroglobulinemia (WM) patients respect to normal B cells. Using the clinically relevant GPER1-selective small-molecule agonist G-1 (also named Tespria), we demonstrate that pharmacological activation of GPER1 leads to G2/M cell cycle arrest and apoptosis both in vitro and in vivo in animal model, even in the context of the protective bone marrow milieu. We report that activation of GPER1 triggers the TP53 pathway, which remains actionable during WM progression. This study identifies a novel druggable target in WM and paves the way for the clinical development of the GPER1 agonist G-1.

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