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PPARg-K107 SUMOylation regulates insulin sensitivity but not adiposity in mice

ABSTRACT: PPARg-K107 SUMOylation regulates insulin sensitivity but not adiposity in mice

PROVIDER: PRJNA492496 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7890180.fastq.gz	Fastqsanger.gz
	SRR7890181.fastq.gz	Fastqsanger.gz
	SRR7890182.fastq.gz	Fastqsanger.gz
	SRR7890183.fastq.gz	Fastqsanger.gz
	SRR7890174.fastq.gz	Fastqsanger.gz

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PPARg-K107 SUMOylation regulates insulin sensitivity but not adiposity in mice

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Project description:Breast cancer is genetically heterogeneous, and recent studies have underlined a prominent contribution of epigenetics to the development of this disease. To uncover new synthetic lethalities with known breast cancer oncogenes, we screened an epigenome-focused short hairpin RNA library on a panel of engineered breast epithelial cell lines. Here we report a selective interaction between the NOTCH1 signaling pathway and the SUMOylation cascade. Knockdown of the E2-conjugating enzyme UBC9 (UBE2I) as well as inhibition of the E1-activating complex SAE1/UBA2 using ginkgolic acid impairs the growth of NOTCH1-activated breast epithelial cells. We show that upon inhibition of SUMOylation NOTCH1-activated cells proceed slower through the cell cycle and ultimately enter apoptosis. Mechanistically, activation of NOTCH1 signaling depletes the pool of unconjugated small ubiquitin-like modifier 1 (SUMO1) and SUMO2/3 leading to increased sensitivity to perturbation of the SUMOylation cascade. Depletion of unconjugated SUMO correlates with sensitivity to inhibition of SUMOylation also in patient-derived breast cancer cell lines with constitutive NOTCH pathway activation. Our investigation suggests that SUMOylation cascade inhibitors should be further explored as targeted treatment for NOTCH-driven breast cancer. We treated MCF10A and NOTCH1 cells with either DMSO or ginkgolic acid 30 uM for 3 days. Two replicates have been analysed for each condition.

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