Identification of TWIST1-associated genomic regions in human breast cancer cell MCF7
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ABSTRACT:
PROVIDER: PRJNA784608 | ENA |
REPOSITORIES: ENA
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Project description:In this study, we aimed to characterize the stimulatory role of TWIST1 in breast cancer cell proliferation, EMT and metastasis, uncover the underlying molecular mechanism, and identify potential therapeutic targets for treating BLBC. RNA-Seq analysis were performed to identify differentially expressed genes influenced by TWIST1 overexpression in breast cancer cell MCF7. Pathway enrichment analysis and gene set enrichment analysis were performed to identify TWIST1-regulated signaling pathways, particually the cancer-associated pathways. ChIP-Seq analysis was further performed to identify TWIST1-associated genomic regions in MCF7-TWIST1 cells. The potential direct target genes of TWIST1 were identified by combined analysis of the gene expression profiling data and ChIP-Seq data.
2022-06-28 | GSE189826 | GEO
Project description:In this study, we aimed to characterize the stimulatory role of TWIST1 in breast cancer cell proliferation, EMT and metastasis, uncover the underlying molecular mechanism, and identify potential therapeutic targets for treating BLBC. RNA-Seq analysis were performed to identify differentially expressed genes influenced by TWIST1 overexpression in breast cancer cell MCF7. Pathway enrichment analysis and gene set enrichment analysis were performed to identify TWIST1-regulated signaling pathways, particually the cancer-associated pathways. ChIP-Seq analysis was further performed to identify TWIST1-associated genomic regions in MCF7-TWIST1 cells. The potential direct target genes of TWIST1 were identified by combined analysis of the gene expression profiling data and ChIP-Seq data.
2022-06-28 | GSE189827 | GEO
Project description:Identification of genes differentially expressed between breast cancer cell lines MCF7-TWIST1 and MCF7-Ctrl
| PRJNA784607 | ENA
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
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.
2016-08-23 | GSE80509 | GEO
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.
2016-08-23 | GSE80334 | GEO
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.
2014-10-28 | E-GEOD-62738 | biostudies-arrayexpress
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.
2016-08-23 | GSE80662 | GEO
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.
2014-10-28 | GSE62738 | GEO