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The PPAR agonist Rosiglitazone induces paracrine signaling in melanoma cells that activate stromal cells and enhances tumor growth.

ABSTRACT: The PPAR agonist Rosiglitazone induces paracrine signaling in melanoma cells that activate stromal cells and enhances tumor growth.

PROVIDER: PRJNA474184 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7247570.fastq.gz	Fastqsanger.gz
	SRR7247561.fastq.gz	Fastqsanger.gz
	SRR7247571.fastq.gz	Fastqsanger.gz
	SRR7247562.fastq.gz	Fastqsanger.gz
	SRR7247572.fastq.gz	Fastqsanger.gz

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The PPAR agonist Rosiglitazone induces paracrine signaling in melanoma cells that activate stromal cells and enhances tumor growth.

Project description:Besides improving insulin sensitivity in type 2 diabetes, the thiazolidinedione family of compounds and the pharmacologic activation of their best characterized target PPARg has been proposed as a therapeutic option for cancer treatment. In the present study, we reveal a new mechanism by which the thiazolidinedione rosiglitazone contributes to tumorigenesis, which limits its therapeutic potential in cancer. We provide evidence that rosiglitazone activates a tumorigenic paracrine communication program in a subset of human melanoma cells, that involves the secretion of cytokines, chemokines and angiogenic factors. This complex blend of paracrine signals activates non-malignant fibroblasts, endothelial cells and macrophages in a tumor-friendly way. In agreement with these data, we show that rosiglitazone promotes human melanoma development in xenografts, through enhanced angiogenesis and inflammation. Together, these findings establish an important tumorigenic action of rosiglitazone in melanoma cells. While studies conducted on cohorts of diabetic patients report overall benefits of TZDs in cancer prevention, we show that exposure of an established tumor to rosiglitazone may be deleterious.

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Effect of PPAR Gamma Agonist Rosiglitazone on Carotid Artery Gene Expression after Knockout of Retinol Binding Protein 7 (RBP7)

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Chronic Rosiglitazone Mouse Aorta

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Transcription profiling of mouse aorta after chronic rosiglitazone treatment

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Analysis of Rosiglitazone therapy on adipose tissue in type 2 diabetic patients

Project description:The goal of this study was to analyse the effect of a 12 weeks treatment with rosiglitazone on gene expression in adipose tissue of type 2 diabetic patients. Diabetic patients were treated with rosiglitazone, agonist of PPAR gamma, during 12 weeks. Adipose tissue biopsies were taken before and after the treatment.

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Identification of an alternative ligand binding pocket in PPAR-γ and its corelated selective agonist for promoting beige adipocyte differentiation

Project description:Pharmacological activation of peroxisome proliferator-activated receptor gamma (PPAR-γ) is a convenient and promising tactic for promoting beige adipocyte biogenesis to combat obesity-related metabolic disorders. However, thiazolidinediones (TZDs), the full agonist of PPAR-γ exhibits severe side effects in animal model and clinical uses. Therefore, it is emerging to develop efficient and safe PPAR-γ modulators for metabolic disease treatment. Here, by utilizing comprehensive methods, we report a previously unidentified ligand binding pocket (LBP) in PPAR-γ and link it to beige adipocyte differentiation. Further virtual screening from 4097 natural compounds based on this novel LBP, we discover NJT-2, a terpenoid compound, can bind to PPAR-γ induce co-activator recruitment and effectively activate PPAR-γ mediated transcription of beige adipocyte program. Importantly, in mouse model, NJT-2 administration efficiently promotes beige adipocyte biogenesis and improve obesity-associated metabolic dysfunction with significant lower adverse effects than those observed in TZD. Our results not only provide an advanced molecular insight into the structural ligand binding details in PPARg, but also develop its linked selective and safe agonist for obesity treatment.

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Comparison of gene expression in CD8 T cells treated with the agonist of PPAR isoforms

Project description:We performed gene expresion analysis of T cell treated with agonist of three isoform of PPAR. This analysis allowed us to explain why the activation of PPAR g is the best in boosting PD-1 blockade efficacy compared with other isoform activation. We demonstrated that activation of the PPAR-γ isoform specifically enhanced PD-1 blockade greater than activation of the other two PPAR isoforms (a and b) in mouse tumor model. Using the microarray assay we found genes that were most differentially regulated by PPAR agonist treatment were with a well-documented role in T cell biology, such as Ddx3y, Ifng, Il17c, Ccr3, Acrv1, Btk and metabolic process such as Pygl, P2rx1, Tph2, Kynu, and Ugt2b37. Therefore, microarray data has been useful to establish that activation of PPAR-g in T cell uniquely modulate genes, which include metabolic as well genes related to immune function.

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Effects of rosiglitazone treatment on lipid composition

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Effect of rosiglitazone treatment on insulin sensitivity in adipose tissue of type 2 diabetic patients

Project description:The goal of this study was to analyse the effect of a 12 weeks treatment with rosiglitazone on insulin sensitivity in the adipose tissue of type 2 diabetic patients. Diabetic patients were submitted to a 3 hours hyperinsulinemic- euglycemic clamp. Adipose tissue biopsies were taken before and after the clamp, labelled A & B respectively. Then, the patients were treated with rosiglitazone, agonist of PPAR gamma, during 12 weeks. After the treatment, all the patients were submitted to a second 3 hours hyperinsulinemic-euglycemic clamp. Adipose tissue biopsies were taken before and after the clamp, labelled C & D respectively.

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RNA-seq with condition Rosiglitazone human adipocyte activated cells - role of PPAR alpha

Project description:RNA-seq with condition Rosiglitazone human adipocyte activated cells - role of PPAR alpha

| PRJEB62125 | ENA