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Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis

ABSTRACT: Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis

PROVIDER: PRJNA290314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2104580.fastq.gz	Fastqsanger.gz
	SRR2104581.fastq.gz	Fastqsanger.gz
	SRR2104572.fastq.gz	Fastqsanger.gz
	SRR2104573.fastq.gz	Fastqsanger.gz
	SRR2104574.fastq.gz	Fastqsanger.gz

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Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis [ChIP-Seq]

Project description:Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis [ChIP-Seq]

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Cbx8 Acts Non-canonically with Wdr5 to Promote Mammary Tumorigenesis.

Project description:Chromatin-mediated processes influence the development and progression of breast cancer. Using murine mammary carcinoma-derived tumorspheres as a functional readout for an aggressive breast cancer phenotype, we performed a loss-of-function screen targeting 60 epigenetic regulators. We identified the Polycomb protein Cbx8 as a key regulator of mammary carcinoma both in vitro and in vivo. Accordingly, Cbx8 is overexpressed in human breast cancer and correlates with poor survival. Our genomic analyses revealed that Cbx8 positively regulates Notch signaling by maintaining H3K4me3 levels on Notch-network gene promoters. Ectopic expression of Notch1 partially rescues tumorsphere formation in Cbx8-depleted cells. We find that Cbx8 associates with non-PRC1 complexes containing the H3K4 methyltransferase complex component WDR5, which together regulate Notch gene expression. Thus, our study implicates a key non-canonical role for Cbx8 in promoting breast tumorigenesis.

| S-EPMC4972459 | biostudies-literature

Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis [ChIP-Seq]

Project description:Here we found that Cbx8 knockdown in MMTV-Myc and MDA-MB-231-Luc cells reduces H3K4me3 mark on Notch-network genes

2016-06-21 | GSE71003 | GEO

Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis [RNA-Seq]

Project description:Here we show that in MMTV-Myc cells (1) MS culture enriches for aggressive breast cancer cells compared to the bulk cells, (2) Cbx8 knockdown reduces Notch-network gene expression.

2016-06-21 | GSE71076 | GEO

Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-06-21 | GSE71077 | GEO

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Project description:Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis [RNA-Seq]

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WDR5 high expression and its effect on tumorigenesis in leukemia

Project description:WD repeat domain 5 (WDR5) plays an important role in various biological functions through the epigenetic regulation of gene transcription. However, the oncogenic effect of WDR5 in leukemia remains largely unknown. Here, we found WDR5 expression is increased in leukemia patients. High expression of WDR5 is associated with high risk leukemia; Patients with WDR5 and MLL1 high expression have poor complete remission rate. We further identified the global genomic binding of WDR5 in leukemic cells and found the genomic co-localization of WDR5 binding with H3K4me3 enrichment. Moreover, WDR5 knockdown by shRNA suppresses cell proliferation, induces apoptosis, inhibits the expression of WDR5 targets, and blocks the H3K4me3 enrichment on the promoter of its targets. We also observed the positive correlation of WDR5 expression with these targets in the cohort study of leukemia patients. Our data reveal that WDR5 may have oncogenic effect and WDR5-mediated H3K4 methylation plays an important role in leukemogenesis.

2016-12-30 | GSE72864 | GEO

Interaction with WDR5 promotes target gene recognition and tumorigenesis by MYC

Project description:We report a comparison of the genome-wide binding patterns of MYC and WDR5, and the effects of a mutation in MYC (WBM) that disrupt the MYC-WDR5 interaction. The experimental design included two distinct experimental strategies. For comparison of genome-wide binding patters of wild-type (WT) and WDR5 binding-deficient (WBM) MYC, HEK293 cells were engineered by retroviral transduction to express either FLAG-tagged WT-MYC, FLAG-tagged WBM-MYC, or an empty vector control ("vec") ChIP was performed on all samples using the anti-FLAG antibody, and co-precipitating DNAs subject to next-generation sequencing. Samples "2514-WPT-1_1", "2514-WPT-5_1" and "2514-WPT-13_1" are three independent biological replicates of ChIPs performed on the "vec" control cells (i.e., those not expressing any exogenous MYC). Samples "2514-WPT-2_1", "2514-WPT-6_1" and "2514-WPT-10_1" are three independent biological replicates of ChIPs performed on the WT-MYC expressing cells. "2514-WPT-3_1", "2514-WPT-7_1" and "2514-WPT-11_1" are three independent biological replicates of ChIPs performed on the WBM-MYC expressing cells. For comparison of these binding patterns with those of WDR5, we performed ChIP in HEK293 cells with either an antibody against WDR5, or with IgG (negative control). Samples "2514-WPT-23_1", "2514-WPT-25_1", and "2514-WPT-27_1" are independent biological replicates of ChIPs performed with the anti-WDR5 antibody. Samples "2514-WPT-24_1", "2514-WPT-26_1", and "2514-WPT-28_1" are independent biological replicates of ChIPs performed with the negative IgG control.

2015-03-30 | E-GEOD-60897 | biostudies-arrayexpress

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Project description:T98G CBX8 KO and WT re-expression RNA-seq analysis to identify potential CBX8 gene targets

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