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Transcriptional profiling of Usp22-WT and Usp22-KO pancreatic tumor cells

ABSTRACT: Transcriptional profiling of Usp22-WT and Usp22-KO pancreatic tumor cells

PROVIDER: PRJNA588235 | ENA |

REPOSITORIES: ENA

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Transcriptional profiling of Usp22-WT and Usp22-KO pancreatic tumor cells

Project description:RNA-seq analysis of sorted Usp22-WT and Usp22-KO tumor cells from subcutaneously implanted mouse pancreatic tumors

2019-11-08 | GSE140088 | GEO

Transcriptional profiling of EPHA2-WT and EPHA2-KO pancreatic tumor cells

Project description:RNA-seq analysis of sorted EPHA2-WT and EPHA2-KO tumor cells from subcutaneously implanted mouse pancreatic tumors

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RNA-Seq of flow-sorted Egfr WT or Egfr KO pancreatic stellate cells (PSCs) and flow-sorted pancreatic tumor organoids following co-culture.

Project description:We investigated changes in transcriptome in Egfr KO PSCs co-cultured with pancreatic tumor organoids compared to Egfr WT PSCs co-cultured with the same pancreatic tumor organoids. We also investigated the changes in transcriptome in pancreatic tumor organoids co-cultured with Egfr WT or Egfr KO PSCs.

2023-11-30 | GSE243838 | GEO

Transcriptional profiling of EPHA2-WT and EPHA2-KO pancreatic tumor cells

Project description:Transcriptional profiling of EPHA2-WT and EPHA2-KO pancreatic tumor cells

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Transcriptional profiling of mouse pancreatic tumor cells I

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Transcriptional profiling of mouse pancreatic tumor cells II

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Secretome and Proteome of WT and CFTR-KO pancreatic duct epithelial cells

Project description:Loss of CFTR function in the pancreatic duct leads to dysregulated luminal pH causing premature activation of digestive enzymes and tissue necrosis. Drastic alterations in pancreatic tissue architecture and cellular composition changes the microenvironment of the islets. Given that CFTR is expressed in the pancreatic ducts, we hypothesized that loss of functional CFTR impacts islet function by modifying the ductal secretome. To this end, we developed a long-term in vitro pancreatic duct epithelial cell culture system and polarized both WT and CFTR-KO (CF) ferret duct epithelial cells. We profiled the apical and basolateral secretome, and the cellular proteome of both WT and CF duct epithelium using quantitative mass spectrometry. Bioinformatic analysis of differentially secreted proteins mapped to their cognate receptors provided a list of putative paracrine interactions that affect islet function. Signaling pathways and upstream regulators that alter the secretome and cellular proteome profile were computationally mined to characterize disease causing mechanisms. In this study, we provide a proteomic roadmap of perturbed autocrine and paracrine signals from the CF pancreatic duct.

2021-05-27 | PXD025126 | Pride

USP22 controls necroptosis by regulating receptor interacting protein kinase 3 ubiquitination

Project description:Dynamic control of ubiquitination by deubiquitinating enzymes is essential for almost all biological processes. Ubiquitin-specific peptidase 22 (USP22) is part of the SAGA complex and catalyzes the removal of monoubiquitination from histone H2B, thereby regulating gene transcription. However, novel roles for USP22 have recently emerged, such as tumor development and cell death. Apart from apoptosis, the relevance of USP22 in other programmed cell death pathways still remains unclear. Here, we describe a novel role for USP22 in controlling necroptotic cell death in a variety of tumor cell lines. Loss of USP22 expression significantly delays TNF/Smac mimetic/zVAD.fmk (TBZ)-induced necroptosis, without affecting TNF-mediated NF-B activation or extrinsic apoptosis. Mass-spectrometric ubiquitin remnant profiling identified lysine 518 of Receptor-interacting protein kinase 3 (RIPK3) as USP22-dependent ubiquitination target during necroptosis induction. Mutation of K518 in RIPK3 reduced necroptosisassociated RIPK3 ubiquitination and amplified necrosome formation and necroptotic cell death. In conclusion, we identify a novel role of USP22 in necroptosis and further elucidate the relevance of ubiquitination as crucial regulator of necroptotic cell death.

2021-05-03 | PXD020909 | Pride

RNA-Seq in WT and KO liver tumor tissues

Project description:RNA-Seq in WT and KO liver tumor tissues

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USP22 supports the aggressive behavior of basal-like breast cancer by stimulating cellular respiration

Project description:Breast cancer (BC), the most frequent tumor entity in women globally, shows a high therapeutic response in early and non-metastatic stages. However, triple-negative BC (TNBC), enriched with cancer stem cells (CSCs), presents significant challenges due to its chemoresistant and metastatic nature. Ubiquitin Specific Proteinase 22 (USP22) has emerged as a key player in promoting CSC functions, contributing to resistance to conventional therapies, tumor relapse, metastasis, and poor survival across various cancers, including BC. The specific role of USP22 in TNBC, however, remains underexplored. In this study, we employed the MMTV-cre, Usp22fl/fl transgenic mouse model to investigate USP22's influence on stem cell-like properties in mammary tissue. High-throughput transcriptomic analyses, combined with publicly available patient data and TNBC culture models, were utilized to elucidate USP22's role in CSC characteristics of TNBC. Our findings reveal that USP22 enhances CSC properties and drug tolerance by supporting oxidative phosphorylation, a key factor in the poor response to conventional therapies in aggressive BC subtypes. The study uncovers a novel tumor-supportive role of USP22 in sustaining cellular respiration, which contributes to the drug-tolerant behavior of HER2+-BC and TNBC cells. This highlights USP22 as a potential therapeutic target, offering new avenues to optimize standard treatments and address the aggressiveness of these malignancies.

2023-12-31 | E-MTAB-13577 | biostudies-arrayexpress

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