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Twist1 gain-of-function studied in 2 normal gastric fibroblast lines

ABSTRACT: Primary human gastric normal fibroblast cultures (NL14 and NL32, repectivley) were establised from 2 gastrectomy specimens. Enforced expression (gain-of-function effect) of Twist1 in 2 gastric normal fibroblasts (NL14 and NL32) showed candidate target genes and CAF markers upregulated by Twist1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62739 | GEO | 2014/10/28

SECONDARY ACCESSION(S): PRJNA265063

REPOSITORIES: GEO

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Twist1 gain-of-function studied in 2 normal gastric fibroblast lines

Project description:Primary human gastric normal fibroblast cultures (NL14 and NL32, repectivley) were establised from 2 gastrectomy specimens. Enforced expression (gain-of-function effect) of Twist1 in 2 gastric normal fibroblasts (NL14 and NL32) showed candidate target genes and CAF markers upregulated by Twist1. Experiment design: 2 normal gastric fibroblasts (NL14 and NL32) were establised and studied for Twist1 gain-of-function.

2014-10-28 | E-GEOD-62739 | biostudies-arrayexpress

Twist1 knockdown in two gastric cancer-associated fibroblast lines

Project description:Primary human gastric cancer-associated fibroblast (CAF) cultures (CAF14 and CAF32) were establised from 2 gastrectomy specimens. Silencing the expression (loss-of-function effect) of Twist1 in CAFs showed candidate target genes regulated by Twist1 and abrogated their tumor-promoting properties. Experiment design: two gastric CAFs (CAF14 adn CAF32, respectively) were establised from two gastric cancer patients and Twist1 knockdown studies were performed using shRNA.

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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. 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

2013-08-20 | E-GEOD-50002 | biostudies-arrayexpress

Impact of ectopic expression of SNAIL2, ZEB2, ZEB1 or TWIST1 on BRAF-target genes in the murine melanocytic melan-a cell line

Project description:We have demonstrated that the oncogenic activation of B-RAF (using a truncated delta-BRAF-ER version inducible with tamoxifen) in the melan-a melanocyte cell line triggers the activation of Zeb1 and Twist1 at the expanse of Zeb2 and Snail2. Enforced maintenance of Zeb2 or Snail2 expression reduces the B-RAF oncogenic potential while ectopic expression of Zeb1 or Twist1 cooperates with B-RAF in melan-a cell transformation. To get an insight into the properties of these embryonic transcription factors, gene expression profiles of melan-a-derived cell lines either expressing a non-activated B-RAF (- tamoxifen) or an activated BRAF (+ tamoxifen) alone or in combination with Snail2, Zeb2, Twist1 or Zeb1 have been established. Melan-a cells were transduced with an activated version of BRAF(delta-BRAF-ER, inducible with tamoxifen) alone or in combination with SNAIL2, ZEB2, ZEB1 or TWIST1. Gene expression profiles before or following BRAF activation (alone or in combination with the embryonic transcription factors) were determined. Ectopic expression of SNAIL2, ZEB2, ZEB1 or TWIST1 on BRAF-target genes in the murine melanocytic melan-a cell line.

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Impact of ectopic expression of SNAIL2, ZEB2, ZEB1 or TWIST1 on BRAF-target genes in the murine melanocytic melan-a cell line

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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.

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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.

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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.

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