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S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation [HeLa RNA-seq]

ABSTRACT: S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation [HeLa RNA-seq]

PROVIDER: PRJNA601211 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10887789_1.fastq.gz	Fastqsanger.gz
	SRR10887789_2.fastq.gz	Fastqsanger.gz
	SRR10887790_1.fastq.gz	Fastqsanger.gz
	SRR10887790_2.fastq.gz	Fastqsanger.gz
	SRR10887791_1.fastq.gz	Fastqsanger.gz

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S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation

Project description:S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation

| PRJNA601208 | ENA

S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation [HeLa RNA-seq]

Project description:Cancer tissues possess less glucose than surrounding normal tissue, because cancer cells predominantly produce energy by glycolysis than oxidative phosphorylation even in the presence of an adequate oxygen supply (Warburg effect). We found a novel compound ALESIA which causes apoptosis of malignant cells at a low glucose condition from an original phenotypic screening. Identified target molecule of ALESIA was Sphingosine-1-phosphate receptor 3 (S1PR3). Being different from the natural ligand, ALESIA selectively stimulated S1PR3-G12 coupling to S1PR3 without suppression by β-arrestin recruitment and continuously promoted NO synthesis. To reduce the enhanced oxidative stress, NAPDH production through pentose-phosphate pathway and resulting consumption of glucose were promoted in ALESIA-treated cells. ALESIA therefore accelerated glucose starvation of cancer cells and preferentially killed them both in vitro and in vivo.

2021-02-08 | GSE143668 | GEO

S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation [MCF-7 RNA-seq]

Project description:S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation [MCF-7 RNA-seq]

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S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation [MCF-7 RNA-seq]

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S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation

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Mapping AT1R biased signaling using proximity-labeling and proteomics identifies diverse actions of biased agonists

Project description:Angiotensin II type 1 receptors (AT1Rs) are one of the most widely studied G protein-coupled receptors. To fully appreciate the diversity in cellular signaling profiles activated by AT1R transducer-biased ligands, we utilized peroxidase-catalyzed proximity labeling to capture proteins in close proximity to AT1Rs in response to six different ligands: Angiotensin II (full agonist), S1I8 (partial agonist), TRV055 and TRV056 (G protein-biased agonists), TRV026 and TRV027 (β-arrestin biased agonists) at 90s, 10min, and 60min after stimulation. We systematically analyzed the kinetics of AT1R trafficking and determined that distinct ligands lead AT1R to different cellular compartments for downstream signaling activation and receptor degradation/recycling. Distinct proximity labelling of proteins from a number of functional classes, including GTPases, adaptor proteins, and kinases were activated by different ligands suggesting unique signaling and physiological roles of the AT1R. Ligands within the same class, i.e. either G protein-biased or -arrestin-biased, shared high similarity in their labelling profiles. Comparison between ligand classes revealed distinct signaling activation such as greater labeling by G protein biased ligands on ESCRT-0 complex proteins that act as sorting machinery for ubiquitinated proteins. Our study provides a comprehensive analysis of AT1R receptor trafficking kinetics and signaling activation profiles induced by distinct classes of ligands.

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Role of Gq/11 and G12/13 signalling in Type II alveolar epithelial cells

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Glucose starvation Bacillus subtilis

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