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Histone H2A T120 phophorylation promotes oncogenic transformation via upregulation of cyclin D1y

ABSTRACT: Histone H2A T120 phophorylation promotes oncogenic transformation via upregulation of cyclin D1y

PROVIDER: PRJNA335832 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3929450_1.fastq.gz	Fastqsanger.gz
	SRR3929450_2.fastq.gz	Fastqsanger.gz
	SRR3929451_1.fastq.gz	Fastqsanger.gz
	SRR3929451_2.fastq.gz	Fastqsanger.gz
	SRR3929452_1.fastq.gz	Fastqsanger.gz

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Histone H2A T120 phophorylation promotes oncogenic transformation via upregulation of cyclin D1 [ChIP-seq]

Project description:It is well known that deregulation of chromatin modifiers, such as histone acetylases and methylases, causes malignancies. However, the possible role of histone phosphorylation in carcinogenesis has not yet been elucidated. Here, we found that histone phosphorylation by itself can be the causal event in carcinogenesis. First, we found that histone H2A T120 is phosphorylated in human cancer cell lines and proved that this phosphorylation is catalyzed by hVRK1. By knocking down VRK1, cyclin D1 was found to be downregulated by loss of H2A T120 phosphorylation and increased H2A K119 ubiquitylation of its promoter region, resulting in impaired cell growth. In human cancer tissues, we found that histone H2A is hyperphosphorylated, with upregulated cyclin D1. Mechanistically, histone H2A T120 phosphorylation and histone H2A K119 ubiquitylation, which repress transcription, are mutually inhibitory, suggesting that histone phosphorylation indirectly activates chromatin. Furthermore, mutated H2A T120D, which mimics phosphorylation, causes elevated H3K4 methylation in the same nucleosome. Subsequently, H3K4R, which functionally mimics H3K4 methylation, increases H3 S10 phosphorylation in the same nucleosome. Finally, both VRK1 and the H2A T120D mutant histone transformed NIH/3T3 cells. This suggests that histone H2A T120 phosphorylation by hVRK1 causes inappropriate gene and protein expression, including upregulated cyclin D1, resulting in carcinogenesis.

2016-10-07 | GSE84583 | GEO

Histone H2A T120 phophorylation promotes oncogenic transformation via upregulation of cyclin D1 [RNA-seq]

2016-10-07 | GSE84527 | GEO

Genome-wide analysis of gene expression regulated by VRK1 kinase in cancer cell lines [Illumina]

Project description:Histone H2A T120 phosphorylation promotes oncogenic transformation via upregulation of cyclin D1

2016-10-07 | GSE84962 | GEO

Mus musculus

Project description:Histone H2A T120 phophorylation promotes oncogenic transformation via upregulation of cyclin D1 [RNA-seq]

| PRJNA329544 | ENA

Homo sapiens

Project description:Histone H2A T120 phophorylation promotes oncogenic transformation via upregulation of cyclin D1 [ChIP-seq]

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Histone H2A T120 phophorylation promotes oncogenic transformation via upregulation of cyclin D1y

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

2016-10-07 | GSE84968 | GEO

Cyclin K and cyclin D1b are oncogenic in myeloma cells

Project description:To study the oncogenic potential of cyclin D1b in the context of mature B cells we generated several cell clones derived from LP-1 MM cell line expressing either cyclin D1b, Myc or cyclin K oncogenes. Transcriptomic analysis allowed us to describe several mechanisms of cyclin D1b- and K-mediated oncogenesis. Three-condition experiment: LP-1cl1, LP-1K and LP-1D1b. Multiple myeloma LP-1 cell lines. Biological replicates: 4 control (LP-1cl1), 4 transfected with cyclin K (Lp-1K) and 4 transfected with cyclin D1b (LP-1D1b) independently grown and harvested. One replicate per array.

2010-04-23 | E-GEOD-15497 | biostudies-arrayexpress

Cyclin K and cyclin D1b are oncogenic in myeloma cells

2010-04-23 | GSE15497 | GEO

Comparison of Normal Prostate Fibroblasts Overexpressing Cyclin D1 and Carcinoma Associated Fibroblasts

Project description:The cyclin D1 oncogene encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the Rb protein and promotes progression through G1 to S phase of the cell cycle. Several prostate cancer cell lines and a subset of primary prostate cancer samples have increased cyclin D1 protein expression. However, the relationship between cyclin D1 expression and prostate tumor progression has yet to be clearly characterized. This study examined the effects of manipulating cyclin D1 expression in either human prostatic epithelial or stromal cells using a tissue recombination model. The data showed that overexpression of cyclin D1 in the initiated BPH-1 cell line increased cell proliferation rate, but did not elicit tumorigenicity in vivo. However, overexpression of cyclin D1 in Normal Prostate Fibroblasts (NPF) that were subsequently recombined with BPH-1 did induce malignant transformation of the epithelial cells. The present study also showed that recombination of BPH-1 + cyclin D1 overexpressing fibroblasts (NPF cyclin D1) resulted in permanent malignant transformation of epithelial cells (BPH-1 NPF-cyclin D1 cells) similar to that seen with Carcinoma Associated Fibroblasts (CAFs). Microarray analysis showed that the expression profiles between CAFs and NPF cyclin D1 cells were highly concordant including cyclin D1 upregulation. These data indicated that the tumor-promoting activity of cyclin D1 may be tissue-specific. Keywords: cyclin D1; stromal-epithelial interactions; prostate cancer; cDNA microarray

2007-09-01 | GSE6936 | GEO

Tumor suppression by Interferon regulatory factor-1 relies on down-regulation of cyclin D1

Project description:Interferons have been ascribed to mediate antitumor effects. IRF-1 is a major target gene of interferons. It inhibits cell proliferation and oncogenic transformation. Here we show that 60% of all mRNAs deregulated by oncogenic transformation mediated by c-myc and H-ras are reverted to the expression levels of non-transformed cells by IRF-1. These include cell cycle regulating genes. Activation of IRF-1 decreases cyclin D1 expression and CDK4 kinase activity concomitant with dephosphorylation of pRb. These effects of IRF-1 are mediated by inhibition of the MEK-ERK pathway and a transcriptional repression of cyclin D1. IRF-1 mediated effects on cell cycle progression were found to be overridden by ectopic expression of cyclin D1. Ablation of cyclin D1 by RNA interference experiments prevents transformation and tumor growth in nude mice. The data demonstrate that cyclin D1 is a key target for IRF-1 mediated tumor suppressive effects. Keywords: NIH3T3 cells, myc, ras, IRF-1, proliferation, transformation, G1/S cell cycle ceckpoint

2006-12-16 | GSE6505 | GEO

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