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Effect of inhibition of VCP on gene expression during colorectal cancer progression of HCT116 cells

ABSTRACT: To investigate the signaling patheway of VCP regulation PD-L1 in colorectal cancer cells, HCT116 cells were treated with CB-5083. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells CB-5083 treatment and untreatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201778 | GEO | 2023/10/18

REPOSITORIES: GEO

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Effect of overexpression of VCP on gene expression during colorectal cancer progression of HCT116 cells

Project description:To investigate the function of VCP in the colorectal cancer progression, we established HCT116 cell lines overexpressing VCP. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells overexpressing VCP and control vector.

2023-07-18 | GSE201660 | GEO

HCT116 cells treated with the p97 inhibitior CB-5083

Project description:The goal of this study was to analyze differential gene expression 8 hr after treatment of CB-5083, a small molecule inhibitor of p97 (VCP), in HCT116 cells grown in culture. DMSO treated cells were compared to cells treated with 1uM CB-5083 after 8 hr.

2015-11-09 | E-GEOD-73588 | biostudies-arrayexpress

Genome-wide maps of chromatin state in HCT116 cells expressing Flag-tagged VCP

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for VCP and Flag in HCT116 cells expressing Flag-tagged VCP.

2023-07-18 | GSE201200 | GEO

HCT116 cells treated with the p97 inhibitior CB-5083

Project description:The goal of this study was to analyze differential gene expression 8 hr after treatment of CB-5083, a small molecule inhibitor of p97 (VCP), in HCT116 cells grown in culture.

2015-11-09 | GSE73588 | GEO

RNAi knock down of VCP in human HeLa cells

Project description:Study of the effects of the VCP knockdown. VCP (p97, yeast cdc48) is a hexameric AAA ATPase involved in various cellular functions including degradation of proteins by the ubiquitin-proteasome system. We examine the consequences of the reduction of VCP levels after RNAi of VCP in HeLa cells. We find ~30 transcripts upregulated in a sequence independent manner. Those transcripts encode proteins involved in endoplasmic reticulum stress, apoptosis, and amino acid starvation.

2006-08-23 | E-MEXP-817 | biostudies-arrayexpress

Proteomic profiling of VCP substrates links VCP to K6-linked ubiquitylation and c-Myc function

Project description:VCP is an evolutionary conserved ubiquitin-dependent ATPase that mediates the degradation of proteins through the ubiquitin-proteasome pathway. Despite the central role of VCP in the regulation of protein homeostasis, identity and nature of its cellular substrates remain poorly defined. Here, we combined chemical inhibition of VCP and quantitative ubiquitin remnant profiling to assess the effect of VCP inhibition on the ubiquitin-modified proteome and to probe the substrate spectrum of VCP in human cells. We demonstrate that inhibition of VCP perturbs cellular ubiquitylation and increases ubiquitylation of a different subset of proteins compared to proteasome inhibition. VCP inhibition globally upregulates K6-linked ubiquitylation that is dependent on the HECT-type ubiquitin E3 ligase HUWE1. We report ~450 putative VCP substrates, many of which function in nuclear processes, including gene expression, DNA repair and cell cycle. Moreover, we identify that VCP regulates the level and activity of the transcription factor c-Myc.

2018-02-08 | GSE107313 | GEO

The differentiation/retrodifferentiation program of human U937 leukemia cells is accompanied by changes of VCP/p97

Project description:A possible functional role of VCP/p97 during differentiation of U937 cells was addressed by siRNA-targeting of VCP/p97. Functional changes in VCP-siRNA-transfected cells following phorbol ester-induced monocytic differentiation have been examind by DNA microarray analysis. Cells transfected with the non-targeting AllStars negative siRNA (Qiagen) served as a reference. Computed

2010-06-29 | E-GEOD-9821 | biostudies-arrayexpress

Neuronal VCP loss of function recapitulates FTLD-TDP pathology

Project description:The pathogenic mechanism by which dominant mutations in VCP cause multisystem proteinopathy (MSP), a rare neurodegenerative disease that presents as fronto-temporal lobar degeneration with TDP-43 inclusions (FTLD-TDP), remains unclear. To explore this, we inactivated VCP in murine postnatal forebrain neurons (VCP cKO). VCP cKO mice have cortical brain atrophy, neuronal loss, autophago-lysosomal dysfunction and TDP-43 inclusions resembling FTLD-TDP pathology. Conditional expression of a single disease-associated mutation, VCP-R155C, in a VCP null background similarly recapitulated features of VCP inactivation and FTLD-TDP, suggesting that this MSP mutation is hypomorphic. Comparison of transcriptomic and proteomic datasets from genetically defined patients with FTLD-TDP reveal that progranulin deficiency and VCP insufficiency result in similar profiles. These data identify a loss of VCP-dependent functions as a mediator of FTLD-TDP and reveal an unexpected biochemical similarity with progranulin deficiency.

2021-06-16 | GSE178257 | GEO

p97/VCP as a therapy target for developing drugs against human coronavirus

Project description:Understanding how human coronavirus dysregulate host proteome during infection in human cells will identify general pathways that are common to coronavirus infection. NMS-873 is an allosteric p97/VCP ATPase inhibitor and was show to have antiviral effect in multiple viruses including SARS-CoV2. We first demonstrated that genetic knock down of p97 reduced HCoV-229E, HCoV-OC43 infection and secretion. To investigate how p97/VCP assists virus infection, we used unbiased quantitative proteomics to compare dysregulated proteomes caused by HCoV-229E, HCoV-OC43 and SARS-CoV2 infection. We then compared dysregulated proteomes after HCoV-229E and HCoV-OC43 infection with and without p97 knockdown. Moreover, we elucidated the impact of p97 on different stages of viral life cycle using two potent p97 inhibitors, CB-5083 and NMS-873 and demonstrate their can block HCoV replication. Together, our data provide insights to repurpose potential cancer drugs that target the essential host protein p97/VCP.

2021-11-03 | PXD026216 | Pride

ASPSCR1-TFE3 reprograms transcription by organizing enhancers around hexameric VCP [HiChIP]

Project description:ChIPseq experiments identify that ASPSCR1-TFE3 defines active enhancers across the genome and co-distributes with VCP/p97. RNAseq after knock-down of ASPSCR1-TFE3 or VCP, inhibition of VCP, or overexpression of each in alveolar soft part sarcoma cell lines demonstrates their co-dependence. HiChIP defines chromatin conformations that surround ASPSCR1-TFE3 targets and are lost on VCP knock-down.

2023-01-01 | GSE162068 | GEO

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