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Altered expression of genes in WDR5 inhibited (by OICR-9429) bladder cancer cells

ABSTRACT: Altered expression of genes in WDR5 inhibited (by OICR-9429) bladder cancer cells

PROVIDER: PRJNA606245 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11073229_1.fastq.gz	Fastqsanger.gz
	SRR11073229_2.fastq.gz	Fastqsanger.gz
	SRR11073230_1.fastq.gz	Fastqsanger.gz
	SRR11073230_2.fastq.gz	Fastqsanger.gz
	SRR11073231_1.fastq.gz	Fastqsanger.gz

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Altered expression of genes in WDR5 knockdown

Project description:WDR5 (WD repeat domain 5) plays an important role in the epigenetic regulation of gene transcription, involing in regulation of embryonic stem cell and cancer cell.Bladder cancer is one of the most common cancers that cause approximately 150,000 deaths per year worldwide.The goal of this study is to identify the target genes of WDR5 in bladder cancer.Our results inditcate that the genes regulated by WDR5 involved in a variety of biological functions, such as proliferation and anti-apoptosis. Bladder cancer cell line UM-UC-3 was transfected with the contol siRNA or two different WDR5 siRNA for 48h. The RNA of the transfected cells was extracted and hybridized on Affymetrix microarrays. We indentified the putative target genes of WDR5 in both WDR5 siRNA by comparing the diferent expressed genes among control, si-WDR5-2 and si-WDR5-3. We futher validated the data of microarray in UM-UC-3 and T24 by RT-qPCR and Western bloting.

2015-02-09 | E-GEOD-59132 | biostudies-arrayexpress

Altered expression of genes in WDR5 knockdown

2015-02-09 | GSE59132 | GEO

Altered expression of genes in WDR5 inhibited (by OICR-9429) bladder cancer cells

Project description:To explore the molecular mechanism underlying OICR-9429-induced WDR5 inhibition in BCa cells, a genome-wide RNA-sequencing was conducted to compare gene expression profiles between OICR-9429 treated T24, UM-UC-3 cells and their control cells

2021-06-24 | GSE145158 | GEO

Altered expression of genes in DANCR knockdown bladder cancer cells

Project description:Altered expression of genes in DANCR knockdown bladder cancer cells

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WDR5 protein interactions at the WIN-site

Project description:The WIN site of WDR5 is a druggable pocket that impairs WDR5 protein function and carries therapeutic potential for treating cancer. This study evaluates the protein interactions affected by small molecule blockade of this surface on WDR5. Inhibited and uninhibited WDR5-containing complexes from HEK293 cells were quantitatively compared by SILAC-based proteomics. Of the high confidence proteins affected by this inhibition, one protein, PDPK1, was investigated further by mass spectrometry for identification of post translational modifications that could influence binding to WDR5.

2021-01-25 | PXD019209 | Pride

Wdr5

Project description:Wdr5

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Proteomics analysis with the WDR5 PROTACs

Project description:Active gene transcription requires accessible chromatin. Post-translational modifications of histone proteins modulate accessibility to target genes, a process that is controlled by multiple chromatin modifying enzymes, remodelers and epigenetic reader proteins. Histone H3K4 methylation serves as hallmark of actively transcribed genes and is introduced by histone methyltransferases (HMTs). For proper function of HMT activity, several adaptor proteins are required. One of these proteins is the WD-repeat containing protein 5 (WDR5) that acts as scaffolding component in HMT complexes and that has been associated with controlling transcription factors including MYC and long non-coding RNAs. The wide influence of dysfunctional HMTs complexes and the typically upregulated MYC levels in diverse tumor types has made WDR5 an attractive cancer drug target. Indeed, protein-protein interface inhibitors for two protein interaction interfaces on WDR5 have been developed. While such compounds only inhibit a subset of WDR5 interactions, chemically induced proteasomal degradation of WDR5 might be an elegant way to target all oncogenic function. In this study, we present the design, synthesis and evaluation of two diverse WDR5 degrader series based on two WIN site binding scaffolds. We show that linker nature and length are essential for successful degradation and strongly influences the degradation rate. In the presented datasets, we determined the intracellular degradation specificity of the WDR5 PROTACs (8g, 6, 17b, 14). We therefore treated MV4-11 cells with 8g and 17b, the corresponding ligands 6 and 14, or DMSO and quantified the induced degradation using a label free approach.

2022-01-27 | PXD025257 | Pride

Altered expression of genes in DANCR knockdown bladder cancer cells

Project description:The prognosis for bladder cancer (BCa) patients with lymph node (LN) metastasis is forlorn and restrainedly improved by current treatment. DANCR is reported to play a role in prostate cancer and liver cancer. However, its function and underlying mechanism in BCa remains unknown. The goal of this study is to identify the target genes of DANCR in bladder cancer. Our results indicate that the genes regulated by DANCR are involved in a variety of biological functions, such as proliferation and metastasis.

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Unannotated microprotein EMBOW switches WDR5 between epigenetic and mitotic roles during cell cycle

Project description:The highly conserved WD40-repeat protein WDR5 is part of multiple functional complexes both inside and outside the nucleus, interacting with the MLL/SET1 histone methyltransferases that catalyze histone H3 lysine 4 (H3K4) di- and tri-methylation (me2,3), and KIF2A, a member of the Kinesin-13 family of microtubule depolymerase. It is currently unclear whether, and how, the distribution of WDR5 between complexes is regulated. Here, we show that an unannotated microprotein dually encoded in the human SCRIB gene regulates the association of WDR5 with epigenetic and KIF2A complexes. We propose to name this alt-protein EMBOW, or microprotein that is the epigenetic to mitotic binder of WDR5. Loss of EMBOW decreases WDR5 interaction with KIF2A, displaces WDR5 from the spindle pole during G2/M phase, and shortens the spindle length, hence prolonging G2/M phase and delaying cell proliferation. On the other hand, loss of EMBOW increases WDR5 interaction with epigenetic complexes, including KMT2A/MLL1, and promotes WDR5 association with chromatin and binding to the target genes, hence increasing H3K4me3 levels of target genes. Together, these results implicate EMBOW as a regulator of WDR5 that switches it between epigenetic and mitotic regulatory roles during cell cycle, explaining how mammalian cells can temporally control the multifunctionality of WDR5.

2023-09-19 | PXD036699 | Pride

Melatonin inhibited tumorigenesis of bladder cancer via suppressing PPARγ/ENO1 mediated glycolysis

Project description:Melatonin inhibited tumorigenesis of bladder cancer via suppressing PPARγ/ENO1 mediated glycolysis

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