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Development of gene expression signatures for neonatal tissues of mice with Usp10 gene knockout

ABSTRACT: Development of gene expression signatures for neonatal tissues of mice with Usp10 gene knockout

PROVIDER: PRJNA816059 | ENA |

REPOSITORIES: ENA

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Development of gene expression signatures for neonatal tissues of mice with Usp10 gene knockout

Project description:To further explore gene expression in neonatal mice with Usp10 gene knockout, we have employed whole genome microarray expression profiling as a discovery platform to identify the pathways or biological processes with the potential to explain the cause of postnatal death of Usp10 knockout mice. Kidney tissues from Usp10 knockout neonates and their littermates were used to be the samples to explore.

2022-03-15 | GSE198574 | GEO

Effect of USP10 knockout using CRISPR on gene expression in MCF7 breast cancer cells

Project description:Using a genome wide shRNa screen we identified the deubiqutinating enzyme USP10 as a potent regualtor of AKT activity. To validate our findings we performed RNA-Seq on MCF7 cells with or without USP10 depletion. In line with our previous observations we demonstrate that PI3k-AKT-mTOR pathway activation is downregualted in our USP10 knockout cells. Our later work shows that this function is mediated through a USP10-GSK3B mediated mechanism resulting in PTEN inactivation. Taken together this work demonstrates the imprtance of USP10 in PI3K pathway regualtion.

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USP10 knockout in human HCT116 cells

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Deubiquitinase USP10 regulates Notch signaling in the endothelium

Project description:Notch signaling is critical for vascular morphogenesis by co-determining the sprouting behavior of endothelial cells. Here, we investigate the function of ubiquitin-specific peptidase 10 (USP10) in regulation of the turnover of the NOTCH1 intracellular domain. HUVEC were transfected with scrambled or USP10 targeting siRNA and then stimulated by treatment with DLL4 or control. RNA for analysis was isolated after 24 hours of DLL4 stimulation.

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Stabilisation of b-Catenin-WNT signalling by USP10 in APC-truncated colorectal cancer drives cancer stemness and enables super-competitor signalling

Project description:The contribution of deubiquitylating enzymes to b-Catenin stabilisation in intestinal stem cells and colorectal cancer (CRC) is poorly understood. Here, we report the deubiquitylase USP10 as APC-truncation- specific regulator enhancer of b-Catenin stability, potentiating WNT signalling pathway in CRC and cancer stem cells. Mechanistically, interaction studies in various CRC cell lines and in vitro binding studies, together with computational modelling, revealed that USP10 binding to b-Catenin is mediated via its USP10 unstructured N-terminus and requires truncated in the absence of full-length APC. Notably, loss of USP10 in CRISPR engineered intestinal organoids reduces tumorigenic properties of CRC cells and organoids, and blocks the super competitor-properties of APC-mutated intestinal cells, elicits induces the expression of differentiation genes, and opposes the APC-truncated phenotype in an intestinal hyperplasia model of D.melanogaster. Taken together, our findings reveal USP10s role in intestinal tumourigenesis by stabilising b-Catenin, leading to aberrant WNT signalling, enhancing cancer cell stemness and implicate the DUB USP10 as a cancer specific therapeutic vulnerability in Apc truncated CRC.

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Effect of USP10 knockout using CRISPR on gene expression in MCF7 breast cancer cells

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USP10-mediated MOF (KAT8) stabilization accelerates the malignant progression of esophageal squamous cell carcinoma via epigenetically activating of ANXA2/Wnt signaling

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