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

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

PROVIDER: PRJNA772779 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16491021.fastq.gz	Fastqsanger.gz
	SRR16491022.fastq.gz	Fastqsanger.gz
	SRR16491023.fastq.gz	Fastqsanger.gz
	SRR16491024.fastq.gz	Fastqsanger.gz
	SRR16491025.fastq.gz	Fastqsanger.gz

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

Project description:We aim to the investigate the role of MST1/2 inhibitor XMU-MP-1 in prostate cancer progression. C4-2 cells were used as the model.

2021-10-26 | GSE186177 | GEO

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

Project description:We aim to the investigate the role of MST1/2 inhibitor XMU-MP-1 in kindy renal clear cell carcinoma (ccRCC) progression. 786-O cells were used as the model.

2022-02-28 | GSE197468 | GEO

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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XMU-MP-1, an inhibitor of the STE20-like MST1/2 kinases of the Hippo signaling pathway, induces hematopoietic tumor cells death

Project description:In this study we have shown that treatment of hematopoietic cells with XMU-MP-1, the inhibitor of MST1/2, the key components of the Hippo signaling pathway, causes inhibition of cell population growth and increased levels of caspase 3/7 activity. RNA-Seq analysis has demonstrated that XMU-MP-1 suppresses the expression of the key cell cycle regulators in the Namalwa cells: E2F family transcription factors, cell division cycle genes (CDC6; CDC7; CDC20; CDC25A,В,С, and CDC45), cyclins CCNА2, CCNB1, CCNB2; MCM2-7, ORC1 and ORC6. At the same time, XMU-MP-1 triggers the activation of the genes regulating apoptosis, necroptosis, and autophagy. XMU-MP-1 increases the expression of the apoptosis activator genes APAF1, caspases 6 and 7, FAS; BBC3, BCL2A1, MOAP1; XAF1. Some Namalwa cells may undergo necroptosis: XMU-MP-1 causes an increase in the expression of the necroptosis activator genes RIPK1, TNFSF10, TRADD, and PEA15, the inhibitor of caspase 8. The expression of the key genes activating autophagy is significantly increased (beclin 1; DEPP1; DAP; VPS18; VPS39, and autophagy regulator AMBRA1). The activation of these three processes in the B-cell tumor population indicates a profound effect of XMU-MP-1 on cell death in hematopoietic tumor cells. The treatment of Namalwa cells with XMU-MP-1 decreases their resistance to doxorubicin. The use of MST1/2 kinase inhibitors in the treatment of hematologic tumors may be extremely promising.

2025-07-02 | GSE279247 | GEO

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

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

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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.

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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

XMU-MP-1, an inhibitor of the STE20-like MST1/2 kinases of the Hippo signaling pathway, induces hematopoietic tumor cells death

Project description:XMU-MP-1, an inhibitor of the STE20-like MST1/2 kinases of the Hippo signaling pathway, induces hematopoietic tumor cells death

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Gene expression analysis of C4-2 cells treated with ACLY inhibitor and Enzalutamide

Project description:This study examined the gene expression effects of treating androgen-deprived C4-2 prostate cancer cells with the ACLY inhibitor BMS-303141 and the AR antagonist enzalutamide.

2017-02-10 | GSE81796 | GEO

Microarray of Mst1/2 deleted epithelial cells from E18.5 mouse lungs

Project description:ShhCre;Mst1/2flx/flx (Mst1/2 D/D) mice were generated to conditionally delete Mst1 and Mst2 from epithelial progenitors during lung morphogenesis. Lungs from E18.5 control and Mst1/2 D/D mice were mechanically and enzymatically dissociated to generate single cell suspension. Epcam(+) cells were isolated using magnetic microbeads. Microarray analysis of mRNAs isolated from Epcam(+) epithelial cells from E18.5 control and Mst1/2 D/D mice was performed to identify transcriptional changes following deletion of the mammalian Hippo kinases (Mst1 and Mst2) from the embryonic lung. The mammalian Hippo kinases, Mst1 and Mst2, were conditionally deleted in epithelial progenitors of the developing lung using ShhCre. Epcam(+) epithelial cells were isolated from the lungs of E18.5 control and Mst1/2 deleted mice. mRNA isolated from Epcam(+) epithelial cells was analyzed by microarray.

2015-01-01 | E-GEOD-61582 | biostudies-arrayexpress

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