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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE135878 | GEO | 2020/01/21

REPOSITORIES: GEO

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

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

| PRJNA560393 | ENA

<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

Transcriptional Profile Tumor Evolution in Metastatic and Non Metastatic MYC driven HCC

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

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TWIST1

Project description:TWIST1

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miRNAs expression in HepG2 hepatocellular carcinoma cell lines: Vector Control vs. Twist1, Bcl-2, and Twist1/Bcl-2 Transfected

Project description:miRNAs profiling of HepG2 cells comparing vector-control treated HepG2 cells with HepG2 cells transfected with Twist1, Bcl-2, and Twist1/Bcl-2 plasmids. Microarray analysis revealed a panel of miRNAs with significant differential expression among these four HCC cell lines.

2017-02-10 | GSE77501 | GEO

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

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ChipSeq of Twist1 and YY1 in PLC-PRF-5 cells

Project description:Epithelial–mesenchymal transition (EMT) is an important mechanism of metastasis and malignant progression of hepatocellular carcinoma (HCC). However, the transcriptional regulation mechanism of EMT remains poorly understood. Some transcriptional co-activators can form phase-separated condensates at super-enhancers that compartmentalize and concentrate the transcription apparatus to drive robust gene expression. Here, we demonstrate that Twist1 and YY1, interact with p300 and form phase-separated local high-concentration interaction hubs at super-enhancers of miRNA-9 and activate its expression to induce EMT and promote the malignant evolution of HCC. Phase separation disrupted by metformin perturbs Twist–YY1 condensates, thereby inhibiting EMT. To explore how the Twist1 complex regulates miR-9 expression by binding SE region, we performed Twist1 ChIP-seq combined with H3K4me3, H3K4me1, H3K27ac, DNAse, p300, and YY1 ChIP-seq data to detect the SEs of miR-9. After metformin treatment, the peak of Twist1/YY1 on miR-9 SE decreased. Metformin specifically affects the binding of Twist1/YY1 to the miR-9 SE region. 1,6-hexanediol, as an aliphatic alcohol, can weaken hydrophobic interactions and inhibit liquid–liquid phase separation by disrupting hydrophobic interactions. In order to prove Twist1/YY1 interaction at these sites requires phase separation, we detect the accessibility of miR-9 SE regions in 1,6-hexanediol-treated cells. The result showed a general decrease in the accessibility of miR-9 super-enhancer regions in 1,6-hexanediol-treated cells and Twist1 / YY1 combines the SE region of miR-9 in the form of phase separation.

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Project description:Transgenic MYC/Twist1 HCC uncergoes tumor regression with persistence of minimal residaul disease (MRD) in the liver upon oncogene deprivation.

2024-08-06 | GSE242743 | GEO

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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