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Transcriptome analysis of control and OTUD1 knockout SKOV3 Cells

ABSTRACT: We have confirmed that high level of OTUD1 is important for retaining ovarian cancer stem cells (OCSCs) property. To investigate the exact mechanism of OTUD1 in the regulation of stemness maintain, we established SKOV3 cells with stable OTUD1 depletion by using sgRNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE232786 | GEO | 2024/01/15

REPOSITORIES: GEO

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Transcriptome analysis of control and OTUD1 knockout T24 Cells

Project description:We have confirmed that OTUD1 interacted directly with Akt and inhibited Akt phosphorylation. To investigate the exact mechanism of OTUD1 in the regulation of Akt signaling pathway, we established T24 cells with stable OTUD1 depletion by using sgRNA.

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Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

Project description:Understanding the molecular mechanisms of pathological vascular remodeling is important for treating cardiovascular diseases and complications. Recent studies have highlighted a role of deubiquitinases in vascular pathophysiology. In this study, we investigated the role of a deubiquitinase, OTUD1, in angiotensin II (Ang II)-induced vascular remodeling. We identified upregulated OTUD1 in the vascular endothelium of Ang II-challenged mice and showed OTUD1 deletion attenuated vascular remodeling, collagen deposition, and EndMT. Conversely, OTUD1 overexpression aggravated these pathological changes both in vivo and in vitro. Mechanistically, SMAD3 was identified as a substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. We found OTUD1 stabilizes SMAD3 and facilitates SMAD3/SMAD4 complex formation and subsequent nuclear translocation through both K48- and K63-linked deubiquitination. OTUD1-mediated SMAD3 activation regulate the transcription of genes involved in vascular EndMT and remodeling in HUVECs. Finally, SMAD3 inhibition reversed OTUD1-promoted vascular remodeling. Our findings demonstrate endothelial OTUD1 promoted Ang II-induced vascular remodeling by deubiquitinating SMAD3. This study identified SMAD3 as a target of OTUD1 and indicates OTUD1 as a potential therapeutic target for the diseases related to vascular remodeling.

2022-12-24 | GSE217304 | GEO

OTUD1 aggravates pathological cardiac hypertrophy through activation of PGAM5-ASK1 signaling pathways

Project description:Deubiquitinating enzymes have gained more and more attention in the field of pathological cardiac hypertrophy. In this study, we explored the role of a deubiquitinase, OTUD1, in the transverse aortic constriction (TAC) induced cardiac hypertrophy. We found the upregulation of OTUD1 in heart tissues of TAC mice. OTUD1 overexpression promoted cardiac hypertrophy, cardiac fibrosis and apoptosis. Conversely, OTUD1 depletion alleviated these pathological changes both in vivo and in vitro. Mechanistically, ASK1 was identified as one substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. Interestingly, OTUD1 didn’t deubiquitinate ASK1, but increased the phosphorylation level of ASK1 during the process of cardiac hypertrophy. We found that PGAM5, the upper stream regulator of ASK1, was stabilized by OTUD1 in a K63 ubiquitin chain dependent way, which reminded us OTUD1 increased the phosphorylation level of ASK1 by deubiquitinating PGAM5. This study identified the OTUD1-ASK1 axis as a potential therapeutic target for pathological cardiac hypertrophy.

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Transcriptome analysis of control and SKOV3 floating sphere cells and sphere differentiated cells

Project description:We initiated this study with the aim of systematically identifying the biomarkers driving tumorigenesis and maintaining tumor dedifferentiation in human ovarian cancer. To achieve that goal, SKOV3 cells were seeded in ultra-low-attachment 96-well plates in DMEM/F12 medium supplemented with 2% B27 serum replacement to allow the formation of floating spheres. Then, these spheres were collected and recultured in a 6-well plate in DMEM with 10% FBS to allow the cells in the spheres to differentiate and attach to the bottom surface, and the genes in which transcription patterns were altered during the transition from OCSCs to differentiated cells.

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Project description:The goals of the study are to compare differently expressed proteins in activated CD4T and OTUD1-deficient CD4T cells. Proteomics was performed with activated CD4T and OTUD1-deficient CD4T cells (n = 3 for each group) to identify the differently expressed proteins and related signaling pathway affected by OTUD1.

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Project description:RNAseq of SKOV3(AA) and SKOV3(CC)

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