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Identification of TWIST1-associated genomic regions in human breast cancer cell MCF7

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE189826 | GEO | 2022/06/28

REPOSITORIES: GEO

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Identification of genes differentially expressed between breast cancer cell lines MCF7-TWIST1 and MCF7-Ctrl

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

Identification of TWIST1-associated genomic regions in human breast cancer cell MCF7

Project description:Identification of TWIST1-associated genomic regions in human breast cancer cell MCF7

| PRJNA784608 | ENA

TWIST1

Project description:TWIST1

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Identification of genes differentially expressed between breast cancer cell lines MCF7-TWIST1 and MCF7-Ctrl

Project description:Identification of genes differentially expressed between breast cancer cell lines MCF7-TWIST1 and MCF7-Ctrl

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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.

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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

Twist1 and Slug mediate H2A.X-regulated epithelial-mesenchymal transition in breast cells

Project description:The epithelial-mesenchymal transition (EMT) is thought to be essential for cancer metastasis. While chromatin remodeling is involved in EMT, histone variants contribution in EMT remains poorly investigated. Recently, we showed that silencing or removal of the histone variant H2A.X induced mesenchymal-like characteristics, including activation of the EMT transcription factors, Slug and ZEB1, in human colon cancer cells. Here, we provide the evidence that H2A.X loss in human non-tumorigenic breast cell line MCF10A results in a robust EMT activation, as substantiated by a genome-wide expression analysis. Cells deficient for H2A.X exhibit enhanced migration and invasion, along with an activation of a set of mesenchymal genes and a concomitant repression of epithelial genes. In the breast model, the EMT-related transcription factor Twist1 cooperates with Slug to regulate EMT upon H2A.X loss. Of interest, H2A.X expression level tightly correlates with Twist1, and to a lesser extent with Slug in the panel of human breast cancer cell lines of the NCI-60 datasets. These new findings indicate that H2A.X is involved in the EMT processes in cells of different origins but pairing with transcription factors for EMT may be tissue specific.

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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.

2012-05-01 | GSE29754 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of wild type, Twist1+/- and Twist1+/- with suture regeneration surgery mice

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived suture transcriptome profiling (RNA-seq) among wild type, Twist1+/- and Twist1+/- with suture regeneration surgery mice Methods: Suture mRNA profiles from one week after induction of seven-month-old wild type, Twist1+/- and Twist1+/- with suture regeneration surgery mice were generated by deep sequencing, in triplicate, using Illumina NextSeq500. Results: Using an optimized data analysis workflow, we mapped about 70 million sequence reads per sample to the mouse genome ( mm10) and identified 43,644 transcripts in the suture of wild type, Twist1+/- and Twist1+/- with suture regeneration surgery mice with Partek E/M workflow.

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

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