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ChIP seq of SiHa RhoC overexpressing cells with RhoC and WDR5 antibodies

ABSTRACT: ChIP seq of SiHa RhoC overexpressing cells with RhoC and WDR5 antibodies

PROVIDER: PRJEB56013 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR10177736_1.fastq.gz	Fastqsanger.gz
	ERR10177736_2.fastq.gz	Fastqsanger.gz
	ERR10177737_1.fastq.gz	Fastqsanger.gz
	ERR10177737_2.fastq.gz	Fastqsanger.gz
	ERR10177738_1.fastq.gz	Fastqsanger.gz

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ChIP seq of SiHa RhoC overexpressing cells with RhoC and WDR5 antibodies

Project description:The aim of the experiment was to identify regions of DNA bound by RhoC and WDR5. SiHa cells overexpressing RhoC were crosslinked, digested with MNase and sonicated. The fragmented DNA that bound to RhoC and WDR5 was pulled down using RhoC and WDR5 antibodies and sequenced using the Illumina HiSeq platform.

2022-12-31 | E-MTAB-12164 | biostudies-arrayexpress

Comparison of transcriptome of SiHa-N (with pcDNA3 backbone vector) and SiHa-R (with RhoC over-expressing plasmid)

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Methylation profiling of RhoC over-expressing SiHa cells (SiHa-R) against SiHa cells with backbone vector alone (SiHa-N)

Project description:Since we have found that the RhoC gene causes extensive changes to gene expression, a methylation array was carried out to determine if the observed transcriptional changes are due to methylation changes in the genome.

2022-12-31 | E-MTAB-12125 | biostudies-arrayexpress

Comparison of transcriptome of SiHa-N (with pcDNA3 backbone vector) and SiHa-R (with RhoC over-expressing plasmid)

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The specific role of RhoC in tumor invasion and metastasis

Project description:The molecules RhoC and RhoA are essential factors for invasion/metastasis of tumor cells proliferation, respectively. RhoC over-expression was especially linked to aggressive cancers, which requires loss of epithelial polarity and deregulation of cellular adhesion. This epithelial-mesenchymal transition (EMT) includes a change in gene expression pattern through several transcription factors, like Snail, ZEB1 or Twist. Here we analyze the potential of RhoC to induce EMT, migration and invasion and to regulate specific genes involved in tumorigenesis. We established stable MCF-10A cell lines with RhoA/RhoC expression under the control of a doxycycline-regulated trans-activator and a transcriptional silencer allowing conditional expression of RhoA and RhoC, respectively. We additionally quantified the transcriptional response from two bacterial toxins: Escherichia coli Cytotoxic Necrotizing Factor 1 (CNF1) and Yersinia pseudotuberculosis Cytotoxic Necrotizing Factor (CNFY) to directly activate the endogenous pool of Rho GTPases and characterized changes in morphology, migration and invasion upon induction of RhoA/RhoC expression or activation by the toxins in MCF-10A grown in two- and three-dimensions. The transcriptome response identified PTGS2 as RhoC specific target genes involved in pro-migratory changes which was experimentally validated.

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ChIP-chip of siGFP- or siHOTTIP-treated foreskin fibroblasts with anti-H3K4me3, anti-H3K27me3, anti-H3K4me2, anti-histone, anti-MLL1, and anti-WDR5 antibodies on HOX tiling array

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RhoC modulates cell junctions and Type I interferon response in aggressive breast cancers

Project description:Metastases are the leading cause of death in cancer patients. RhoC, a member of the Rho GTPase family, has been shown to facilitate metastasis of aggressive breast cancer cells by influencing motility, invasion, and chemokine secretion, but as yet there is no integrated model of the precise mechanism of how RhoC promotes metastasis. A common phenotypic characteristic of metastatic cells influenced by these mechanisms is dysregulation of cell-cell junctions. Thus, we set out to study how RhoA- and RhoC-GTPase influence the cell-cell junctions in aggressive breast cancers. We demonstrate that CRISPR-Cas9 knockout of RhoC in SUM 149 and MDA 231 breast cancer cells results in increased normalization of junctional integrity denoted by junctional protein expression/colocalization. In functional assessments of junction stability, RhoC knockout cells have increased barrier integrity compared to wild-type cells as measured by the FITC-Dextran leakage assay, and increased cell-cell adhesion as measured by fluorimetric centrifugation assay. Whole transciptome RNA sequencing demonstrate decreased expression of Type I interferon-stimulated genes in RhoC knockout cells compared to wild-type, and subsequent treatment with interferon-alpha resulted in significant increases in adhesion and decreases in invasiveness of wild-type cells and a dampened response to interferon-alpha stimulation with respect to adhesion and invasiveness in RhoC knockout cells. We delineate a key role of RhoC-GTPase in modulation of junctions and response to interferon, which supports inhibition of RhoC as a potential anti-invasion therapeutic strategy.

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Wdr5

Project description:Wdr5

| PRJNA739648 | ENA