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The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [gene expression]

ABSTRACT: WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis We analysed whether WDR5 siRNAs modulate gene expression

ORGANISM(S): Homo sapiens

PROVIDER: GSE69861 | GEO | 2015/12/31

SECONDARY ACCESSION(S): PRJNA286992

REPOSITORIES: GEO

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The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [gene expression]

Project description:WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis We analysed whether WDR5 siRNAs modulate gene expression Neuroblastoma BE(2)-C cells were treated with control siRNA, WDR5 siRNA-1, and WDR5 siRNA-2 for 40 hours, and subjected to differential gene expression studies with Affymetrix microarrays.

2015-12-31 | E-GEOD-69861 | biostudies-arrayexpress

The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [ChIP-Seq]

Project description:WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis Using ChIP-Seq, We profiled key epigenetic marks H3K4 trimethylation in BE(2)-C neuroblastoma cells transfected with control siRNA or WDR5 siRNA-1 at N-Myc target gene promoters The results showed knockdown WDR5 significantly reduced H3K4me3 at 93.2% of N-Myc binding promoters, but only at 53.5% of N-Myc non-binding promoters. Identification of Histone H3K4 trimethylation and N-Myc binding sites in BE(2)-C cells transfected with control siRNA or WDR5 siRNA-1.

2015-12-31 | E-GEOD-70098 | biostudies-arrayexpress

The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [ChIP-Seq]

2015-12-31 | GSE70098 | GEO

The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-31 | E-GEOD-70099 | biostudies-arrayexpress

The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma

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

2015-12-31 | GSE70099 | GEO

WDR5 facilitates recruitment of N-MYC to conserved gene targets in neuroblastoma cell lines

Project description:Collectively, the MYC family of oncoprotein transcription factors are overexpressed or deregulated in more than half of all malignancies. The ability of MYC proteins to access chromatin is fundamental to their role in promoting oncogenic gene expression programs in cancer and this function depends on MYC-cofactor interactions. One such cofactor is the chromatin regulator WDR5, which in models of Burkitt’s lymphoma facilitates recruitment of the c-MYC protein to chromatin at select target genes associated with protein synthesis, allowing for tumor progression and maintenance. However, beyond Burkitt’s lymphoma it is unknown whether these observations extend to other cancers or MYC family members, and whether WDR5 can be deemed as a “universal” MYC recruiter. Here, we focus on N-MYC amplified neuroblastoma to determine the extent of colocalization between N-MYC and WDR5 on chromatin while also demonstrating that like c-MYC, WDR5 can facilitate recruitment of N-MYC to known conserved WDR5-bound genes. We conclude based on this analysis that N-MYC and WDR5 colocalize invariantly across cell lines at predicted sites of facilitated recruitment associated with protein synthesis genes. Surprisingly, we also identify N-MYC-WDR5 cobound genes that are associated with DNA repair and cell cycle processes. Dissection of chromatin binding characteristics of N-MYC and WDR5 at all cobound genes reveals that sites of facilitated recruitment are inherently different than most N-MYC-WDR5 cobound sites. Our data reveals that WDR5 acts as a universal MYC recruiter at a small cohort of previously identified genes and highlights novel biological functions that may be coregulated by N-MYC and WDR5 to sustain the neuroblastoma state.

2023-06-19 | GSE222157 | GEO

A Role for WDR5 in Integrating Threonine 11 Phosphorylation to Lysine 4 Methylationon Histone H3 and in Prostate Cancer

Project description:Upon androgen stimulation, PKN1-mediated histone H3 threonine 11 phosphorylation (H3T11P) promotes AR target genes activation. However, the underlying mechanism is not completely understood. Here, we show that WDR5, a subunit of the SET1/MLL complex, interacts with H3T11P and this interaction facilitates the recruitment of the SET1/MLL complex and subsequent H3K4 trimethylation (H3K4me3). Using ChIP-seq, we find that androgen stimulation results in a six-fold increase in the number of H3T11P-marked regions and induces WDR5 colocalization to one third of H3T11P-enriched promoters, thus establishing a genome-wide relationship between H3T11P and recruitment of WDR5. Accordingly, PKN1 knock-down or chemical inhibition severely blocks WDR5 association and H3K4me3 on AR target genes. Finally, WDR5 is critical in prostate cancer cell proliferation, and is hyperexpressed in human prostate cancers. Together, these results identify WDR5 as a critical epigenomic integrator of histone phosphorylation and methylation and a major driver of androgen-dependent prostate cancer cell proliferation. Identification of Histone 3 threonine 11 phosphorylation (H3T11P) marks and WDR5 binding sites in LNCaP cells treated with R1881 ligand (androgen) or solvent control.

2014-07-01 | E-GEOD-55279 | biostudies-arrayexpress

A Role for WDR5 in Integrating Threonine 11 Phosphorylation to Lysine 4 Methylationon Histone H3 and in Prostate Cancer

2014-07-01 | GSE55279 | 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

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.

2015-03-30 | GSE60897 | GEO

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