Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA methylation variations are required for reversible EMT induced by cancer-associated fibroblasts in PCa cells

ABSTRACT: DNA methylation variations are required for reversible EMT induced by cancer-associated fibroblasts in PCa cells

PROVIDER: PRJEB14150 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

DNA methylation variations are required for reversible EMT induced by cancer-associated fibroblasts in PCa cells

Project description:Epithelial-to-mesenchymal transition (EMT) and cancer stem cells play relevant roles in metastasis and drug resistance in castration-resistant PCa. Conditioned-media from Cancer-Associated Fibroblasts from two patients with aggressive PCa induce EMT, reversible DNA methylation and transcriptional variations in androgen independent PC3, but not in androgen dependent LN-CaP cells. Focal CpG islands hyper-methylation associated to transcriptional repression of epithelial markers occurs together with widespread hypo-methylation, including promoters of EMT and stemness regulating genes resulting in their transcriptional activation. Remarkably, DNA methylation and transcription patterns are entirely reverted upon exposure to serum-free medium (mesenchymal-to-epithelial transition). DNMT3A is required for de novo methylation and silencing of CDH1 and GRHL2, the ZEB1 direct repressor, while its knock-down prevents EMT entry. These unprecedented results highlight that CAF-released factors induce reversible DNA methylation patterns required for transcriptional variations essential for EMT and stemness in androgen independent PCa cells, suggesting that similar plasticity might occur in tumour microenvironment.

2017-03-09 | E-MTAB-4752 | biostudies-arrayexpress

DNA methylation variations are required for reversible EMT induced by cancer-associated fibroblasts in PCa cells

Project description:Epithelial-to-mesenchymal transition (EMT) and cancer stem cells play relevant roles in metastasis and drug resistance in castration-resistant prostate cancer (PCa). Conditioned-media from Cancer-Associated Fibroblasts from two patients with aggressive PCa induce EMT, reversible DNA methylation and transcriptional variations in androgen independent PC3, but not in androgen dependent LN-CaP cells. Focal CpG islands hyper-methylation associated to transcriptional repression of epithelial markers occurs together with widespread hypo-methylation, including promoters of EMT and stemness regulating genes resulting in their transcriptional activation. Remarkably, DNA methylation and transcription patterns are entirely reverted upon exposure to serum-free medium (mesenchymal-to-epithelial transition). DNMT3A is required for de novo methylation and silencing of CDH1 and GRHL2, the ZEB1 direct repressor, while its knock-down prevents EMT entry. These unprecedented results highlight that CAF-released factors induce reversible DNA methylation patterns required for transcriptional variations essential for EMT and stemness in androgen independent PCa cells, suggesting that similar plasticity might occur in tumour microenvironment. This submission contains data and metadata from the methylation profiling by array of PC-3 cells treated with conditioned media from Human prostate fibroblasts (HPFs) and cancer associated fibroblasts (CAFs).

2017-03-03 | E-MTAB-4753 | biostudies-arrayexpress

RNA sequence analysis of stable versus reversible EMT events and the resultant metastases

Project description:The ability of breast cancer cells to transiently transition between epithelial and mesenchymal states is critical to complete the metastatic process. In contrast, induction of epithelial-mesenchymal transition (EMT) through the acquisition of drug persistence is a more stable event. Herein, we utilize Her2 transformed human mammary epithelial (HMLE) cells to compare a reversible model of EMT induced by TGF-beta to a stable mesenchymal phenotype induced by chronic exposure to the ErbB kinase inhibitor, lapatinib. Indeed, only a TGF-beta cells capable of returning to an epithelial phenotype resulted in long bone metastasis (BM). These four cell populations were anylzed by RNA sequencing.

2019-06-04 | GSE115255 | GEO

RNA sequence analysis of stable versus reversible EMT events and the resultant metastases

Project description:RNA sequence analysis of stable versus reversible EMT events and the resultant metastases

| PRJNA474381 | ENA

Gene expression in human prostate cancer (PCa) cell lines upon HIC1 silencing

Project description:To explore the role of HIC1 silencing in regulating PCa EMT development, Human Gene Expression Microarrays were searched for altered genes upon silencing HIC1 expression in C4-2B and DU145 cells. According to fold-change screening betweenHIC1-silenced and its respective control cells, both up-regulated and down-regulated genes were shown. Human PCa cell lines C4-2B and DU145 were transfected with lenti-virus (shRNA targeting HIC1 and respective control). HIC1-silenced cells were respectively noted as C4-2B-shHIC1 and DU145-shHIC1. Their respective control cells were respectively noted as C4-2B-shctrl and DU145-shctrl.

2016-03-03 | E-GEOD-78850 | biostudies-arrayexpress

PCa-LINES

Project description:PCa-LINES: Ribo-minus RNA-seq of 4 patient samples and 2 PCa cell lines

| EGAS00001004613 | EGA

Gene expression in human prostate cancer (PCa) cell lines upon HIC1 silencing

2016-03-03 | GSE78850 | GEO

Phased gene expression and chromatin accessibility during progressive EMT and MET linked to dynamic CTCF engagement (ATAC-Seq)

Project description:We report the chromatin accessibility alterations and gene expression changes in TGFB-induced and -withdrawn reversible EMT in MCF10A mammary epithelial cells

2021-12-01 | GSE145849 | GEO

Phased gene expression and chromatin accessibility during progressive EMT and MET linked to dynamic CTCF engagement (RNA-Seq)

Project description:We report the chromatin accessibility alterations and gene expression changes in TGFB-induced and -withdrawn reversible EMT in MCF10A mammary epithelial cells

2020-12-01 | GSE145850 | GEO

CNV Identification: Prostate Cancer (PCa) vs Benign Prostatic Hyperplasia (BPH) Human DNA Samples

Project description:Copy number variations (CNVs) in the human genome have been linked to various carcinomas including prostate cancer (PCa). This study was conducted to identify CNVs in high grade PCa. We performed a pilot genome-wide CNV analysis in 36 subjects (18 high grade PCa and 18 benign prostatic hyperplasia) using array comparative genomic hybridization (aCGH) technique. Array results were validated using PCR-based copy number counting method. A total of 339 CNV regions were found to be unique to PCa subjects in this cohort (P < 0.05). Data segregation and filtering revealed six putative CNV loci associated with susceptibility to PCa. Of these, four were rare (1q21.3, 15q15, 3q27.2 and 7p12.1) and one was a novel copy number gain (12q23.1), harbouring genes such as the ARNT, THBS1, SLC5A8 and DDC which are crucial in the p53 and cancer pathways. Another CNV was a loss at 8p11.21 which contains the SFRP1 gene from the Wnt signalling pathway, known for its interaction with androgen receptors as reported for urological malignancy. Cross comparison analysis with genes already known to be associated with PCa revealed significant CNVs involved in crucial biological processes that elicit cancer pathogenesis via cytokine production, disease progression through endothelial cell proliferation and xenobiotic metabolism. In conclusion, these findings suggest that the CNV regions identified could provide an insight into the development of high grade PCa.

2018-12-18 | GSE79402 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data