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Genome wide expression change by MCF-7 cells treated with MST1/2 inhibitor

ABSTRACT: Genome wide expression change by MCF-7 cells treated with MST1/2 inhibitor

PROVIDER: PRJNA693878 | ENA |

REPOSITORIES: ENA

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Genome wide expression change by MCF-7 cells treated with MST1/2 inhibitor

Project description:We aim to the investigate the role of MST inhibitor in breast cancer progression. MCF-7 cells were used as the model.

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Genome wide expression change by C4-2 cells treated with MST1/2 inhibitor XMU-MP-1

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Genome wide expression change by 786-O cells treated with MST1/2 inhibitor XMU-MP-1

Project description:Genome wide expression change by 786-O cells treated with MST1/2 inhibitor XMU-MP-1

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Genome wide expression change by C4-2 cells treated with MST1/2 inhibitor XMU-MP-1

Project description:Genome wide expression change by C4-2 cells treated with MST1/2 inhibitor XMU-MP-1

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Genome-wide H3K27ac deposition in MCF-7 cells treated with p300 KAT inhibitor A-485

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2021-06-16 | GSE172174 | GEO

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RNA sequencing data from wild type and Mst1/2 knockout esophageal epithelium

Project description:Hippo signaling regulates the homeostasis of multiple organs. Mst1 and Mst2 (Mst1/2) are critical components of the Hippo signaling pathway. Here, we utilized RNA sequencing to determine the transcriptional change in the esophageal epithelium upon Mst1/2 deletion. The analysis of gene expression profiles allows us to understand the role of Mst1/2 in the regulation of various biological processes in the esophageal epithelium.

2024-02-26 | GSE248501 | GEO

Leukotriene B4 receptor 1 antagonist in combination with kinase MST1/2 inhibitor has potential for treatment of myocardial infarction

Project description:Timely inhibition of inflammation and initiation of resolution are important for the repair of injured tissues. Pharmacological inhibition of mammalian STE20-like protein kinase 1/2 (MST1/2) with XMU-MP-1 might augment tissue regeneration and repair by suppressing apoptosis and increasing cell proliferation. However, MST1 has anti-inflammatory activity, inhibition of which may result in therapy failure. Here, we identified an approach with the potential to overcome this limitation by protecting against cardiac inflammation resulting from inhibition of MST1 in macrophages. We found exacerbation of cardiac dysfunction in LysMCre-mediated Mst1/2-deficient mice after myocardial infarction (MI). This effect was attributed to a shift of macrophage subtypes from those expressing Cxcl2 and Cd163 toward those with Ccl2 and Ccl4 expression. Mass spectrometry identified leukotriene B4 (LTB4) as the lipid mediator that was upregulated in the absence of MST1. We found that MST1 phosphorylated 5-lipoxygenase (5-LOX) at its T218 residue, disrupting the interaction between 5-LOX and 5-LOX-activating protein, and resulting in reduction of LTB4 production. By contrast, a 5-LOXT218A variant showed no response to MST1. Moreover, treatment of peritoneal macrophages with LTB4 or with medium conditioned by Mst1-deficient macrophages resulted in high Ccl2 and Ccl4 expression and low Cxcl2 and Cd163 expression, except when the cells were co-treated with the LTB4 receptor 1 (BLT1) antagonist CP105696. Furthermore, CP105696 ameliorated cardiac dysfunction in LysMCre-mediated Mst1/2-deficient mice and enhanced cardiac repair in wild-type mice treated with XMU-MP-1 after MI. The combination of an MST1/2 inhibitor and a BLT1 antagonist represents a promising strategy for combatting the effects of MI.

2021-12-13 | GSE181935 | GEO

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