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PARP inhibition induces cytotoxicity in mESCs by activating endogenous retroviruses.

ABSTRACT: PARP inhibition induces cytotoxicity in mESCs by activating endogenous retroviruses.

PROVIDER: PRJNA702474 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13732900_1.fastq.gz	Fastqsanger.gz
	SRR13732900_2.fastq.gz	Fastqsanger.gz
	SRR13732901_1.fastq.gz	Fastqsanger.gz
	SRR13732901_2.fastq.gz	Fastqsanger.gz
	SRR13732902_1.fastq.gz	Fastqsanger.gz

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PARP inhibition induces cytotoxicity in mESCs by activating endogenous retroviruses.

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Farnesyl diphosphate synthase inhibition remodels the tumor immune microenvironment by activating endogenous retroviruses

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Farnesyl diphosphate synthase inhibition remodels the tumor immune microenvironment by activating endogenous retroviruses

Project description:Farnesyl diphosphate synthase inhibition remodels the tumor immune microenvironment by activating endogenous retroviruses

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Project description:PARP inhibition and the effect on Arabidopsis thaliana high light tolerance

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Project description:Poly(ADP-ribose) polymerase-2 (PARP-2) is acknowledged as a DNA repair enzyme; however, recently metabolic properties had been attributed to it. Hereby, we examined the metabolic consequences of PARP-2 ablation in liver. Microarray analysis of PARP-2 knockdown HepG2 cells revealed the dysregulation of lipid and cholesterol metabolism genes. Induction of cholesterol biosynthesis genes stemmed from the enhanced expression of sterol-regulatory element binding protein (SREBP)-1. We revealed that PARP-2 is a suppressor of the SREBP-1 promoter, therefore ablation of PARP-2 induces SREBP-1 expression and consequently cholesterol synthesis. PARP-2-/- mice had higher SREBP-1 expression that was translated into enhanced hepatic and serum cholesterol levels. PARP-2 silencing was performed employing shPARP-2 (small hairpin) and scPARP-2 (scrambled) shRNA by lentiviral delivery (Sigma) using 40 MOI lentiviruses coding shRNA sequence against PARP-2.

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Farnesyl diphosphate synthase inhibition remodels the tumor immune microenvironment by activating endogenous retroviruses

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Combinatorial treatment with PARP and MAPK inhibitors overcomes phenotype switch-driven drug resistance in advanced melanoma

Project description:Metastatic melanoma is either intrinsically resistant or rapidly acquires resistance to targeted therapy treatments, such as MAPK inhibitors. A leading cause of resistance to targeted therapy is a dynamic transition of melanoma cells from a proliferative to a highly invasive state, a phenomenon called phenotype switching. Mechanisms regulating phenotype switching represent potential targets for improving treatment of melanoma patients. Using a drug screen targeting chromatin regulators in patient-derived 3D MAPK inhibitor-resistant melanoma cell cultures, we discovered that PARP inhibitors restore sensitivity to MAPK inhibitors, independent of DNA damage repair pathways. Integrated transcriptomic, proteomic, and epigenomic analyses demonstrated that PARP inhibitors induce lysosomal autophagic cell death, accompanied by enhanced mitochondrial lipid metabolism that ultimately increases antigen presentation and sensitivity to T-cell cytotoxicity. Moreover, transcriptomic and epigenetic rearrangements induced by PARP inhibition reversed EMT-like phenotype switching, which redirected melanoma cells toward a proliferative and MAPK inhibitor-sensitive state. The combination of PARP and MAPK inhibitors synergistically induced cancer cell death both in vitro and in vivo in patient-derived xenograft models. Therefore, this study provides a scientific rationale for treating melanoma patients with PARP inhibitors in combination with MAPK inhibitors to abrogate acquired therapy resistance.

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