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MYC and Twist1 cooperate to drive metastasis by eliciting crosstalk between cancer and innate immunity

ABSTRACT: MYC and Twist1 cooperate to drive metastasis by eliciting crosstalk between cancer and innate immunity

PROVIDER: PRJNA560393 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9973510.fastq.gz	Fastqsanger.gz
	SRR9973511.fastq.gz	Fastqsanger.gz
	SRR9973512.fastq.gz	Fastqsanger.gz
	SRR9973513.fastq.gz	Fastqsanger.gz
	SRR9973514.fastq.gz	Fastqsanger.gz

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MYC and Twist1 cooperate to drive metastasis by eliciting crosstalk between cancer and innate immunity

Project description:Comparative transcriptional profiling of MYC driven HCC and MYC/Twist1 driven HCC during tumor progression, regression and recurrence.

2020-01-21 | GSE135878 | GEO

<i>MYC</i> and <i>Twist1</i> cooperate to drive metastasis by eliciting crosstalk between cancer and innate immunity.

Project description:Metastasis is a major cause of cancer mortality. We generated an autochthonous transgenic mouse model whereby conditional expression of MYC and Twist1 enables hepatocellular carcinoma (HCC) to metastasize in >90% of mice. MYC and Twist1 cooperate and their sustained expression is required to elicit a transcriptional program associated with the activation of innate immunity, through secretion of a cytokinome that elicits recruitment and polarization of tumor associated macrophages (TAMs). Systemic treatment with Ccl2 and Il13 induced MYC-HCCs to metastasize; whereas, blockade of Ccl2 and Il13 abrogated MYC/Twist1-HCC metastasis. Further, in 33 human cancers (n = 9502) MYC and TWIST1 predict poor survival (p=4.3×10-10), CCL2/IL13 expression (p<10-109) and TAM infiltration (p<10-96). Finally, in the plasma of patients with HCC (n = 25) but not cirrhosis (n = 10), CCL2 and IL13 were increased and IL13 predicted invasive tumors. Therefore, MYC and TWIST1 generally appear to cooperate in human cancer to elicit a cytokinome that enables metastasis through crosstalk between cancer and immune microenvironment.

| S-EPMC6959993 | biostudies-literature

TWIST1

Project description:TWIST1

| PRJNA784600 | ENA

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 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 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

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.

2020-08-04 | GSE155562 | GEO

TWIST1 direct targets during embryonic stem cell differentiation

Project description:Twist1 encodes a basic helix-loop-helix (bHLH) transcription factor and is a key regulator of craniofacial development. Mutations of TWIST1 gene in human are associated with Saethre-Chotzen syndrome (SCS), a developmental disorder characterized by facial and skull malformations, which are phenocopied by Twist1-null heterozygous mice. Mechanisms that dictate the tissue-specificity of Twist1 in regulating distinct transcriptional targets in different craniofacial cell types remain to be determined. Our work using mass-spectrometry and co-expression analysis in cell lines and embryonic head tissues has revealed that the most prevalent forms of TWIST1 were homodimers and heterodimers with E-proteins (TCF3,TCF4 and TCF12). RNA-seq analysis of embryoid bodies expressing tethered TWIST-E-protein dimers, and ChIP-seq profiling of TWIST1 genome-wide binding sites revealed mechanisms of TWIST1 functional regulation. This study highlighted the pleiotropic roles of TWIST1 dimers in development and revealed a potential molecular mechanism underpinning Twist1-related developmental defects of craniofacial tissues.

2020-03-12 | GSE130253 | GEO

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

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