Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The dynamics of chromatin accessibility during EMT

ABSTRACT: The power of our genome-wide survey lies in that we were able to query chromatin accessibility changes concurrently with those in DNA methylation. We identified both opening and closing events, predominantly independent of DNA methylation, in both systems. Our results have powerful implications for future basic and clinical research on this developmental process and its resurfacing during cancer cell metastasis. To address epigenetic changes that mediate EMT, we used two models in the human system: EMT induced by the transcriptional repressor Twist as well as EMT induced by TGF-beta. We performed AcceSssIble on these cells at several time points through the course of the transition and identified genes that need to be repressed to allow for the process.

ORGANISM(S): Homo sapiens

SUBMITTER: Xiaojing Yang

PROVIDER: E-GEOD-63366 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

An EMT-driven alternative splicing program occurs in human breast cancer and modulates cellular phenotype.

Project description:Regulation of cell-cell junction formation and regulation of cell migration were enriched among EMT (Epithelial-Mesenchymal Transition)-associated alternatively splicing events. Our analysis suggested that most EMT-associated alternative splicing events are regulated by one or more members of the RBFOX, MBNL, CELF, hnRNP or ESRP classes of splicing factors. The EMT alternative splicing signature was confirmed in human breast cancer cell lines, which could be classified into basal and luminal subtypes based exclusively on their EMTassociated splicing pattern. Expression of EMT-associated alternative mRNA transcripts was also observed in primary breast cancer samples, indicating that EMT-dependent splicing changes occur commonly in human tumors. The functional significance of EMT-associated alternative splicing was tested by expression of the epithelial-specific splicing factor ESRP1 or depletion of RBFOX2 in mesenchymal cells, both of which elicited significant changes in cell morphology and motility towards an epithelial phenotype, suggesting that splicing regulation alone can drive critical aspects of EMT-associated phenotypic changes. The molecular description obtained here may aid in the development of new diagnostic and prognostic markers for analysis of breast cancer progression. Examination of transcriptomes of HMLE/Twist-ER before and after induction of EMT by tamoxifen

2011-07-15 | E-GEOD-30290 | biostudies-arrayexpress

BLUEPRINT WP4: Methylation study of germinal-center derived B-cell lymphoma cell lines as part of whole epigenomes

Project description:INFINIUM HUMAN METHYLATION 450 BEAD CHIP ANALYSIS OF germinal-center derived B-cell lymphoma cell line DNA (cell lines: BL2, DG75, JVM2, Karpas422, SUDHL5, U266, Z138)

2014-12-25 | E-MTAB-3184 | biostudies-arrayexpress

MET after transient Twist activation results in de novo gain of malignant traits

Project description:During Epithelial-Mesenchymal Transition (EMT), apical-basal polarized epithelial cells are converted to front-to-back polarized mesenchymal cells that only form loose cell-cell adhesions. These phenotypic changes are accompanied by acquisition of increased motility and invasiveness. EMT programs are orchestrated by pleiotropic transcription factors (TFs), such as Twist1 and Snail1 and effect morphogenetic steps during embryogenesis, including mesoderm formation and neural crest migration. EMTs have also been implicated in the acquisition of aggressive traits by carcinoma cells, including the ability to complete several steps of the metastatic cascade as well as propagation of the tumor by single cells (clonogenicity), a defining trait of tumor-initiating or cancer stem cells. However, the molecular links between the expression of EMT-TFs, the process of EMT and acquisition of clonogenicity remain obscure. Using inducible Twist1 or Snail1 expressed in CD24-positive mammary epithelial cells, we show that clonal growth in anchorage independence and EMT are induced sequentially and independently: clonogenic potential is induced prior to EMT and requires transient TF-activity. By contrast, EMT depends on continuous TF-activation over a longer period. In 3D-collagen assays, continuous Twist1 activity suppresses colony formation, whereas transient activation induces highly invasive growth independently of EMT. In conclusion, our results demonstrate that transient Twist1 activation suffices to drive tumor progression of CD24-positive breast epithelial cells, assessed by invasive as well as anchorage-independent clonal growth, whereas chronic Twist1 exposure can suppress these traits of aggressive tumor cells. We performed gene expression microarray analysis on CD24high and CD24negative populations derived from HMLE-Twist1-ER or HMLE-Snail1-ER cell lines upon various culture conditions

2015-07-02 | E-GEOD-61206 | biostudies-arrayexpress

Genome-wide methylation profiling in granulosa lutein cells of women with polycystic ovary syndrome (PCOS)

Project description:Our study is based on the hypothesis that PCOS can be explained by an integrated, epigenetic model, whereby environmental factors modify the effect of susceptibility genes and influence the clinical heterogeneity that is characteristic of the syndrome during adult life. With the aim to understand the molecular mechanisms underlying PCOS, we report results from a case-control, genome-wide methylation study using human DNA from granulosa lutein cells.

2019-03-01 | E-MTAB-6672 | biostudies-arrayexpress

Epigenome analysis of genomic DNA isolated from whole blood of non-diabetic control and type-2 diabetic individuals

Project description:DNA methylation profiling of whole blood using Illumina's Infinium HumanMethylation27 Beadchip array. The dataset encompasses profiles of 12 non-diabetic control blood donors and 12 type-2 diabetic (T2D) individuals. Bisulfite converted DNA from 24 blood samples were hybridised to the Illumina Infinium HumanMethylation27 Beadchip

2012-04-22 | E-GEOD-34008 | biostudies-arrayexpress

RNA-seq of two human mammary epithelial cell lines (HMLE and HMLE-Twist-ER) treated with 4-hydroxytamoxifen vs control

Project description:Immortalized non-cancerous human mammary epithelial cells (HMLE) were transfected to express the murine fusion protein Twist1-estrogen receptor(point mutation G525R) (HTER). Twist1-mediated gene expression is activated by stimulation with 4-hydroxytamoxifen for several days and induces an epithelial-mesenchymal transition (EMT) in HTER cells. In breast cancer, EMT equips cancer cells for metastasis and therapy resistance. As control, HTER cells were treated with vehicle (methanol). As additional controls, HMLE cells were stimulated with 4-hydroxytamoxifen or methanol, respectively. Prior to RNA sequencing, EMT-undergoing HTER cells were sorted by fluorescence-activated cell sorting (FACS) based on E-Cadherin and CD44 surface protein levels into three populations, epithelial (E), hybrid epithelial-mesenchymal (EM), and mesenchymal (M): E-Cadherin_high_CD44_low (E), E-Cadherin_medium_CD44_medium (EM), and E-Cadherin_low_CD44_high (M).

2021-03-24 | E-MTAB-9365 | biostudies-arrayexpress

Whole DNA methylome of an extramedullary multiple myeloma patient derived orthotopic xenograft

Project description:A patient derived orthotopic xenograft (PDOX) was generated from a patient with an 53 aggressive extramedullary multiple myeloma (EMM) to study in-depth genetic and epigenetic events and drug responses related to extramedullary disease. Whole DNA methylome of the EMM PDOX was also evaluated and compared with a published dataset of 101 newly-diagnosed and chemotherapy-naïve MM patients and normal plasma cells (NPC) (Agirre et al., 2015) A rather balanced proportion of hyper/hypomethylated sites different to previously reported widespread hypomethylation in MM was observed.

2021-06-25 | E-MTAB-10654 | biostudies-arrayexpress

Methylation profiling by array of 108 clear cell renal cell carcinoma

Project description:A Cartes d'Identite des Tumeurs (CIT) project from the French Ligue Nationale Contre le Cancer (<a href=\\ttp://cit.ligue-cancer.net/\\ target=\\_blank\\>http://cit.ligue-cancer.net</a>). Selecting patients with metastatic clear-cell renal cell carcinoma (m-ccRCC) who might benefit from treatment with targeted tyrosine kinase inhibitors (TKIs) is a challenge. Our aim was to identify molecular markers associated with outcome in m-ccRCC patients treated with sunitinib.\

2016-02-26 | E-MTAB-3274 | biostudies-arrayexpress

Global methylation analysis of development and progression of colorectal carcinoma

Project description:Colorectal tumorigenesis proceedes through well defined clinical stages assoicated with charateristic mutations. Besides genetic alterations, epi-driver genes that are aberrantly expressed in cancers in a fashion that confers a seletive growth advantage can also contribute to tumor evolution. To gain a global view of methylation patterns in normal and maliganant colorectal epithelia, we performed genome-wide DNA methylation analysis on DNAs from 48 fresh frozen CRC samples at different stages of CRC progression. We used IlluminaHumanMethylation450 Beadchip to get a broad view of genome-wide DNA methylationdata during CRC progression and identified significantly differentially methylated genes during CRC progression A total of 48 macro-dissected tissues including normal colon tissue, adenomas, carcinomas and metastases were collected by the Department of Pathology at the University of Virginia under the supervision of an experienced pathologist. DNA was extracted and run on IlluminaHumanMethylation450 Beadchip by Expression Analyisis.

2016-05-13 | E-GEOD-77954 | biostudies-arrayexpress

Recurrent TCF12 mutations in anaplastic oligodendroglioma

Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net: Anaplastic oligodendrogliomas (AOs) are rare primary brain tumors which are generally incurable with few treatment targets identified. Most oligodendrogliomas have chromosome 1p/19q co-deletion and IDH mutation. We analyzed 51 AOs by whole-exome and/or transcriptome sequencing identifying previously reported frequent somatic mutations in CIC and FUBP1 genes. We also identified recurrent mutations in TCF12 (11% of IDHmut-codel) which encodes basic helix-loop-helix (bHLFH) transcription factor 12 which is an oligodendrocyte-related transcription factor in IDHmut-codel tumors. Strikingly, the somatic mutations (encoding E548R and R602M substitutions) have not been reported previously in cancer but are identical to germline mutations causing craniosynostosis. Incorporating TCGA data on 43 AO tumors also implicates functional mutation of SMARCA4, NOTCH1, NOTCH2, SETD2, RBPJ and ARID1A/1B. These data are compatible with the combined deregulation of metabolism, chromatin organization/remodeling and Notch-pathway genes in AO oncogenesis. Our analysis provides further insights into the unique and shared pathways driving AO and new targets for therapeutic intervention.

2015-06-15 | E-MTAB-2767 | biostudies-arrayexpress

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