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

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

PROVIDER: PRJNA733664 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14685300_1.fastq.gz	Fastqsanger.gz
	SRR14685300_2.fastq.gz	Fastqsanger.gz
	SRR14685301_1.fastq.gz	Fastqsanger.gz
	SRR14685301_2.fastq.gz	Fastqsanger.gz
	SRR14685254_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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.

2021-06-07 | GSE175787 | GEO

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 junction protein expression/colocalization. In functional assessments of junction stability, RhoC knockout cells have increased barrier integrity and increased cell-cell adhesion compared to wild-type cells. Whole exome RNA sequencing and targeted gene expression profiling 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.

| S-EPMC8428533 | biostudies-literature

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.

2017-10-22 | GSE98244 | GEO

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

Elevated expression of wildtype RhoC promotes ErbB2- and Pik3ca-induced mammary tumor formation

Project description:Copy number gains in genes coding for Rho activating exchange factors as well as losses affecting genes coding for RhoGAP proteins are common in breast cancer, suggesting that elevated Rho signaling may play an important role. Extra copies and overexpression of RhoC also occur, although a role for RhoC overexpression in driving tumor formation has not been assessed in vivo. To this end, we report on the development of a Rosa26 (R26)-targeted Cre-conditional RhoC overexpression mouse (R26-RhoC). This mouse was crossed to two models for ERBB2/NEU+ breast cancer: one based on expression of an oncogenic ErbB2/Neu cDNA downstream of the endogenous ErbB2 promoter (FloxNeoNeuNT), the other, a metastatic model that is based on high-level expression from MMTV regulatory elements (NIC). RhoC overexpression dramatically enhanced mammary tumor formation in FloxNeoNeuNT mice but showed a more subtle effect in the NIC line, which forms multiple mammary tumors after a very short latency. Many mammary tumors that form in FloxNeoNeuNT mice show selection for increased NeuNT expression linked to high-level amplification of the ErbB2/NeuNT locus. In contrast, NeuNT overexpression did not require high-level amplification of ErbB2/NeuNT in RhoC-FloxNeoNeuNT lesions. RhoC overexpression also enhanced mammary tumor formation in a model for breast cancer induced by Pik3ca(H1047R). The transforming effect of RhoC was associated with epithelial/mesenchymal transition (EMT) in ErbB2/NeuNT and Pik3ca-H1047R systems. Thus, RhoC copy number gains with resultant overexpression contribute to breast tumor formation and/or progression.

2024-04-11 | GSE249601 | GEO

The landscape of alternative splicing in aggressive prostate cancers

Project description:The landscape of alternative splicing in aggressive prostate cancers

| PRJNA594270 | ENA

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

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

| PRJEB56013 | ENA

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

Project description:Since RhoC is known to be involved in various tumour phenotypes, a transcriptome analysis was carried out with RhoC over-expressing cells to identify the genes altered by RhoC over-expression.

2022-12-31 | E-MTAB-12162 | biostudies-arrayexpress

5-hydroxymethylation highlights the heterogeneity in keratinization and cell junctions in head and neck cancers

Project description:5-hydroxymethylation highlights the heterogeneity in keratinization and cell junctions in head and neck cancers

| PRJNA602545 | ENA

HSP90 specific nIR probe identifies aggressive prostate cancers: a translational study from preclinical models to a human pilot study

Project description:Current screening modalities for prostate cancer rely on serologic testing for PSA and transrectal biopsy; however, many prostate cancers behave indolently.Because aggressively growing tumors depend on oncogenic drivers, we hypothesized that we could identify early, but aggressive prostate cancer,by an imaging modality targeting Hsp90, a chaperone for many molecules involved in oncogenic signaling. Previously we observedgreater avidity ofa probe,consisting of a near infrared dye tethered to an Hsp90 inhibitor,for cancers with greatermetastatic potential. We now report that an Hsp90 inhibitor-linked near infrared dye with greater tissue penetration could detect prostate cancers in preclinical models and in a phase I human clinical trial. These data, demonstrating specific uptake into aggressive tumors, in conjunction with our prior observations on photodynamic therapy guided by Hsp90 expression support a theranostic approach todetect and treatearly aggressive prostatecancers.

2022-01-01 | GSE164865 | GEO

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