Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Twist-box mutation on gene expression induced by Twist1 overexpression

ABSTRACT: Twist1 is a transcription factor that induces EMT and drives metastasis in prostate cancer. We examined global gene expression in Myc-CaP mouse prostate cancer cells following overexpression of Twist1 and the Twist1 mutants F191G, AQA, and DQD. 15 total samples were analysed, with 3 replicates of 5 groups: Twist1-WT, Twist1-AQA, Twist1-DQD, Twist1-F191G, and vector control. We performed the comparisons: WT > VEC, F191G > VEC. Samples were normalized by Twist1 expression in addition to normal

ORGANISM(S): Mus musculus

SUBMITTER: Russell Williams

PROVIDER: E-GEOD-50002 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Effect of Twist-box mutation on gene expression induced by Twist1 overexpression

Project description:Twist1 is a transcription factor that induces EMT and drives metastasis in prostate cancer. We examined global gene expression in Myc-CaP mouse prostate cancer cells following overexpression of Twist1 and the Twist1 mutants F191G, AQA, and DQD.

2013-08-20 | GSE50002 | GEO

TWIST1

Project description:TWIST1

| PRJNA784600 | ENA

The twist box domain is required for Twist1-induced prostate cancer metastasis.

Project description: Not available

| S-EPMC3833995 | biostudies-literature

Differential regulation of Twist1-responsive genes in 4T1 cells

Project description:Twist1 variants including wildtype Twist1, a non-phosphorylatable mutant Twist1/S42A and a phospho-mimicking mutant Twist1/S42D were expressed in 4T1 cells in which the endogenous Twist1 was depleted. We wanted to use microarray analysis to evaluate those genes that are differentially regulated by Twist1 variants. All cell lines were grown to 70% confluency and total RNA was isolated with Qiagen kit. Each sample was prepared as triplicates. Parental 4T1 cells were used as control.

2012-04-30 | E-GEOD-29754 | biostudies-arrayexpress

Identification of TWIST1 transcriptional targets in the cranial mesoderm [E8_5]

Project description:TWIST1, a basic helix-loop-helix transcription factor is essential for the development of cranial mesoderm and cranial neural crest-derived craniofacial structures. Our previous work showed that, in the absence of TWIST1, some cells within the cranial mesoderm adopt an abnormal epithelial configuration. Here, we show by transcriptome analysis that loss of TWIST1 in the cranial mesoderm is accompanied by a reduction in the expression of genes that are associated with cell-extracellular matrix interactions and the acquisition of mesenchymal characteristics. By comparing the transcriptional profiles of cranial mesoderm-specific Twist1 loss-of-function mutant and control mouse embryos, we identified a set of genes that are both TWIST1-dependent and predominantly expressed in the mesoderm. By ChIP-seq in a cell line model of a TWIST1-dependent mesenchymal state, we identified, among the downstream genes, three direct transcriptional targets of TWIST1: Ddr2, Pcolce and Tgfbi. Our findings show that the mesenchymal properties of the cranial mesoderm is likely to be regulated by a network of TWIST1 targets genes that influence the extracellular matrix and cell-matrix interactions, and collectively they are required for the morphogenesis of the craniofacial structures. For microarray analysis of CM-CKO embryos, embryo heads of four genotypes were collected at E8.5 (5-7 somites) and E9.5 (18- 20 somites): CM-CKO (Twist1flox/del; Mesp1Cre/+), CM-Het (Twist1flox/wt; Mesp1Cre/+), Het (Twist1flox/del; Mesp1+/+) and Control (Twist1flox/wt; Mesp1+/+). Sample sizes for E8.5 embryos were as follows: Control, n=4 CM-CKO, n=4; Het, n=3; CM-Hets, n=3).

2016-08-23 | E-GEOD-80334 | biostudies-arrayexpress

Identification of TWIST1 transcriptional targets in the cranial mesoderm [E9_5]

Project description:TWIST1, a basic helix-loop-helix transcription factor is essential for the development of cranial mesoderm and cranial neural crest-derived craniofacial structures. Our previous work showed that, in the absence of TWIST1, some cells within the cranial mesoderm adopt an abnormal epithelial configuration. Here, we show by transcriptome analysis that loss of TWIST1 in the cranial mesoderm is accompanied by a reduction in the expression of genes that are associated with cell-extracellular matrix interactions and the acquisition of mesenchymal characteristics. By comparing the transcriptional profiles of cranial mesoderm-specific Twist1 loss-of-function mutant and control mouse embryos, we identified a set of genes that are both TWIST1-dependent and predominantly expressed in the mesoderm. By ChIP-seq in a cell line model of a TWIST1-dependent mesenchymal state, we identified, among the downstream genes, three direct transcriptional targets of TWIST1: Ddr2, Pcolce and Tgfbi. Our findings show that the mesenchymal properties of the cranial mesoderm is likely to be regulated by a network of TWIST1 targets genes that influence the extracellular matrix and cell-matrix interactions, and collectively they are required for the morphogenesis of the craniofacial structures. For microarray analysis of CM-CKO embryos, embryo heads of four genotypes were collected at E8.5 (5-7 somites) and E9.5 (18- 20 somites): CM-CKO (Twist1flox/del; Mesp1Cre/+), CM-Het (Twist1flox/wt; Mesp1Cre/+), Het (Twist1flox/del; Mesp1+/+) and Control (Twist1flox/wt; Mesp1+/+). Sample sizes for E9.5 were as follows: Control, n=3; CM-CKO, n=4; Het, n=4; CM-Het, n=4). RNA was extracted using the RNeasy Micro kit (Qiagen) and samples sent to the Australian Genome Research Foundation for labelling and hybridization.

2016-08-23 | E-GEOD-80509 | biostudies-arrayexpress

TWIST1 methylation by SETD6 selectively antagonizes LINC-PINT expression in Glioblastoma multiforme

Project description:Glioblastoma multiforme (GBM) is the most common and aggressive malignant brain tumor among adults, which is characterized by high invasion, migration and proliferation abilities. One important process that contributes to the invasiveness of GBM is the epithelial to mesenchymal transition (EMT). EMT is regulated by a set of defined transcription factors which tightly regulate this process, among them is the basic helix-loop-helix family member, TWIST1. Here we show that TWIST1 is methylated on lysine-33 at chromatin by SETD6, a methyltransferase with expression levels correlating with poor survival in GBM patients. RNA-seq analysis in U251 GBM cells suggested that both SETD6 and TWIST1 regulate cell adhesion and migration processes. We further show that TWIST1 methylation attenuates the expression of the long-non-coding RNA, LINC-PINT, thereby suppressing EMT in GBM. Mechanistically, TWIST1 methylation represses the transcription of LINC-PINT by increasing the occupancy of EZH2 and the catalysis of the repressive H3K27me3 mark at the LINC-PINT locus. Under un-methylated conditions, TWIST1 dissociates from the LINC-PINT locus, allowing the expression of LINC-PINT which leads to increased cell adhesion and decreased cell migration. Together, our findings unravel a new mechanistic dimension for selective expression of LINC-PINT mediated by TWIST1 methylation.

2022-08-12 | PXD029361 | Pride

TWIST1 regulated human melanoma transcriptome

Project description:TWIST1 is known to play a role in the metastatic progression of melanoma. However, the range of TWIST1 targets is poorly charachterized. Here microarray analysis was used to define the TWIST1 regulated transcriptome in the human melanoma cell line WM793.

2019-04-03 | GSE128955 | GEO

TWIST1 expression is associated with high-risk Neuroblastoma and promotes Primary and Metastatic Tumor Growth

Project description:In this study, merging in silico transcriptomic data and in situ TMA studies, we first highlighted the clinical significance and the value as prognostic factors of the embryonic TFs TWIST1 and TWIST2, thus linking their level of expression with the outcome of NB patients. Secondly, using NB cells knocked out for the TWIST1 protein, we studied the biological impact of TWIST1 in tumors xenografts. The expression of TWIST1 was associated with enhanced primary and secondary tumor growth capacity in immunocompromised mice. Furthermore, tumors expressing TWIST1 were portrayed by a more aggressive phenotype, characterized by the presence of spindle shaped cells and the destruction of the ECM collagen fibers. Finally, the transcriptional signature deregulated by TWIST1 was found to have a clinical significance in human primary tumors and resulted to be able to activate the TME in ortho-derived xenograft. This dataset reports analyses that studied the impact of knockout of the TWIST1 protein on the secretome of the neuroblastoma cell line mentioned above.

2022-01-10 | PXD024200 | Pride

Differential regulation of Twist1-responsive genes in 4T1 cells

2012-05-01 | GSE29754 | 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