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Genome-wide expression analysis of VprBP knockdown in DU145 cells

ABSTRACT: VprBP has been implicated in transcriptionally silent chromatin formation and cell cycle regulation, but the molecular basis underlying such effects remains unclear. To investigate the role of VprBP on gene regulation, genme-wide gene expression analysis is carried out in DU145 cells expressing either control shRNA or VprBP shRNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE50414 | GEO | 2013/11/07

SECONDARY ACCESSION(S): PRJNA217449

REPOSITORIES: GEO

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Genome-wide expression analysis of VprBP knockdown in DU145 cells

Project description:VprBP has been implicated in transcriptionally silent chromatin formation and cell cycle regulation, but the molecular basis underlying such effects remains unclear. To investigate the role of VprBP on gene regulation, genme-wide gene expression analysis is carried out in DU145 cells expressing either control shRNA or VprBP shRNA. Total RNA was isolated from mock- or VprBP-depleted DU145 cells

2013-11-07 | E-GEOD-50414 | biostudies-arrayexpress

Controls and CNTN1 overexpression in DU145 cells and CNTN1 knockdown in DU145 cell-derived prostate cancer stem-like cells

Project description:Prostate cancer stem-like cells were derived from DU145 cells as suspension spheres. DU145 cells were transduced with a CNTN1 over expressing retroviral vector and a control empty vector. DU145 spheres were transduced using a retroviral-based shRNA vector against CNTN1 and a scrambled control shRNA viral vector. Both cell lines were cultured over a couple of passages before RNA was collected.

2016-02-12 | E-MTAB-4118 | biostudies-arrayexpress

Gene expression profiling from human prostate cancer PC3 or DU145 cells with control or ESS2 knockdown.

Project description:PC3 and DU145 cells stably transduced with control or ESS2 shRNA were established. Total RNA was isolated from 5x 10^6 cells of each

2023-08-09 | GSE173998 | GEO

VprBP directs epigenetic gene silencing through H2A phosphorylation in colon cancer

Project description:Histone modification is aberrantly regulated in cancer and generates an unbalanced state of gene transcription. VprBP, a recently identified kinase, phosphorylates histone H2A on threonine 120 (T120) and is involved in oncogenic transcriptional dysregulation; however, its specific role in colon cancer is undefined. Here we show that VprBP is overexpressed in colon cancer and directly contributes to epigenetic gene silencing and cancer pathogenesis. Mechanistically, the observed function of VprBP is mediated through H2AT120 phosphorylation (H2AT120p)-driven transcriptional repression of growth regulatory genes, resulting in a significantly higher proliferative capacity of colon cancer cells. Our preclinical studies using organoid and xenograft models demonstrate that treatment with VprBP inhibitor B32B3 impairs colonic tumor growth by blocking H2AT120p and reactivating transcriptional program resembling that of normal cells. Collectively, our work describes VprBP as a master kinase contributing to the development and progression of colon cancer, making it a new molecular target for novel therapeutic strategies.

2021-10-06 | GSE180282 | GEO

Phosphorylation and stabilization of EZH2 by VprBP trigger aberrant gene silencing in colon cancer

Project description:Our recent work has shown that VprBP is overexpressed in colon cancer and phosphorylates histone H2AT120 to drive epigenetic gene inactivation and oncogenic transformation. We have extended these observations by investigating whether VprBP also phosphorylates non-histone proteins as an additional mechanism linking its kinase activity to colon cancer development. We now demonstrate that VprBP directly phosphorylates EZH2 at T367 to augment its nuclear stabilization and enzymatic activity in colon cancer cells. Consistent with this mechanistic role, VprBP-mediated EZH2 phosphorylation leads to elevated levels of H3K27me3 and altered expression of growth regulatory genes in cancer cells. Furthermore, our preclinical studies using organoid and xenograft models revealed that EZH2 requires phosphorylation for its oncogenic function, which may have therapeutic implications for gene reactivation in colon cancer cells. Together, our data define a new mechanism underlying VprBP-driven colonic tumorigenesis by linking VprBP-mediated EZH2 phosphorylation to EZH2 stability that is crucial for establishing H3K27me3 and gene silencing program.

2023-03-28 | GSE192489 | GEO

Targeting USP2 regulation of VPRBP-mediated degradation of p53 and PD-L1 for cancer therapy

Project description:Here, we identify the USP2 (ubiquitin specific peptidase 2)-VPRBP (viral protein R binding protein) axis as a new pathway for p53 regulation. Like Mdm2 (Mouse double minute 2), VPRBP is a potent repressor of p53 but VPRBP stability is controlled by USP2. Interestingly, the USP2-VPRBP axis is also involved in PD-L1 (programmed death-ligand 1) regulation. Strikingly, in immunocompetent mouse models, the combination of a small-molecule USP2 inhibitor and anti-PD1 monoclonal antibody leads to complete regression of the tumors expressing wild-type p53. In contrast to Mdm2, knockout of the USP2 gene in mice has no obvious effect in normal tissues. Moreover, no obvious toxicity is observed upon the USP2 inhibitor treatment in vivo as Mdm2-mediated regulation of p53 remains intact. These data demonstrate that USP2 is a promising target to induce potent tumor suppression without obvious toxicity. Our study reveals a new strategy for p53-based therapy by circumventing the toxicity issue.

2023-03-15 | PXD040473 | Pride

Targeting USP2 regulation of VPRBP-mediated degradation of p53 and PD-L1 for cancer therapy

2023-03-15 | PXD040477 | Pride

Expression data from prostate cancer cell lines LNCap (androgen dependent) and DU145 (androgen independent), transfected with Pin1 or control siRNA

Project description:Pin1 inhibiton exerts anti-oncogenic effects on LNCaP and DU145 cells despite the gene regulation patterns by Pin1 were different in both cells. We investigated how Pin1 modulates the gene expressions in the androgen-dependent as well as the androgen-independent prostate cancer cell lines For the knockdown of human Pin1, the siRNAs against Pin1 (Pin1 shRNA-1: 5’-CGGCAACAGCAGCAGUGGUGGCAAA-3’ and Pin1 shRNA-2: 5’-GCCCUGGAGCUGAUCAACGGCUACA-3’) and control siRNA were purchased from Invitrogen (Stealth/siRNA duplex oligoribonucleotides)

2015-04-01 | E-GEOD-67457 | biostudies-arrayexpress

RNA-Seq of DU145 cell line upon knockdown of YAP, TAZ, or YAP/TAZ

Project description:Transcriptome analysis of prostate cancer patient derived organoid DU145 cell line upon knockdown of YAP, TAZ, or YAP/TAZ mediated by siRNAs

2022-03-24 | GSE199347 | GEO

Epigenome analysis of DU145 samples [II]

Project description:The Illumina Infinium 850k Human DNA methylation BeadChip was used to obtain DNA methylation profiles in DU145 cell samples. Samples included normal, PLK1 knockdown and UHRF1 knockdown DU145 cell samples. Each sample is repeated three times.

2022-10-31 | GSE185400 | GEO

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