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Transcriptome analysis of TWIST1 sgRNA-treated human tumor endothelial cells

ABSTRACT: The global RNA expression was assayed on human glioblastoma-derived tumor endothelial cells (ECs) treated with CRISPR/sgRNA targeting Twist1 or control sequence.

ORGANISM(S): Homo sapiens

PROVIDER: GSE221950 | GEO | 2023/02/15

REPOSITORIES: GEO

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CUT&RUN analysis of TWIST1 binding chromatin profile in human tumor endothelial cells

Project description:The global chromatin binding profile of TWIST1 was assayed on human glioblastoma-derived tumor endothelial cells (ECs).

2023-02-15 | GSE221949 | GEO

Transcriptome analysis of tumor and normal brain endothelial cells

Project description:The global RNA expression was assayed with endothelial cells (ECs) derived from human glioblastoma and normal brains using RNAseq.

2023-02-17 | GSE199375 | GEO

Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression

Project description:Uncontrolled accumulation of pulmonary artery smooth muscle cells (PASMC) to the distal pulmonary arterioles (PAs) is one of the major characteristics of pulmonary hypertension (PH). Cellular senescence contributes to aging and lung diseases associated with PH and links to PH progression. However, the mechanism by which cellular senescence controls vascular remodeling in PH is not fully understood. The levels of senescence marker, p16INK4A and senescence-associated β-galactosidase (SA-β-gal) activity are higher in PA endothelial cells (ECs) isolated from idiopathic pulmonary arterial hypertension (IPAH) patients compared to those from healthy individuals. Hypoxia-induced accumulation of α-smooth muscle actin (αSMA)-positive cells to the PAs is attenuated in p16fl/fl-Cdh5(PAC)-CreERT2 (p16iΔEC) mice after tamoxifen induction. We have reported that endothelial TWIST1 mediates hypoxia-induced vascular remodeling by increasing platelet-derived growth factor (PDGFB) expression. Transcriptomic analyses of IPAH patient or hypoxia-induced mouse lung ECs reveal the alteration of senescence-related gene expression and their interaction with TWIST1. Knockdown of p16INK4A attenuates the expression of PDGFB and TWIST1 in IPAH patient PAECs or hypoxia-treated mouse lungs and suppresses accumulation of αSMA–positive cells to the supplemented ECs in the gel implanted on the mouse lungs. Hypoxia-treated mouse lung EC-derived exosomes stimulate DNA synthesis and migration of PASMCs in vitro and in the gel implanted on the mouse lungs, while p16iΔEC mouse lung EC-derived exosomes inhibit the effects. These results suggest that endothelial senescence controls αSMA–positive cell proliferation and migration in PH through TWIST1-PDGFB signaling.

2022-10-15 | PXD033549 | Pride

Effects of PAK4 knockdown on gene expression in glioblastoma-associated endothelial cells

Project description:PAK4 was knocked down in human glioblastoma (GBM)-associated endothelial cells (ECs) using CRISPR-Cas9/gRNA. RNA was isolated and analyzed by RNAseq. The effects of PAK4 knockout on gene expression were determined.

2020-09-13 | GSE154133 | GEO

Effects of PHGDH CRISPR knockout on gene expression in glioblastoma-associated endothelial cells

Project description:PHGDH was knocked out in human glioblastoma (GBM)-associated endothelial cells (ECs) using CRISPR-Cas9/gRNA. RNA was isolated and analyzed by RNAseq. The effects of PHGDH knockout on gene expression were determined.

2023-02-17 | GSE199376 | GEO

Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression

Project description:Uncontrolled accumulation of pulmonary artery smooth muscle cells (PASMC) to the non-muscularized distal pulmonary arterioles (PAs) is one of the major characteristics of pulmonary hypertension (PH). Cellular senescence contributes to aging and lung diseases associated with PH and links to PH progression. However, the mechanism by which cellular senescence controls vascular remodeling in PH is not fully understood. Here, we have demonstrated that endothelial senescence mediates PH pathology by increasing platelet-derived growth factor (PDGFB) expression. The levels of senescence markers p16INK4A and senescence-associated β-galactosidase (SA-β-gal) are higher in PA endothelial cells (ECs) isolated from IPAH patients compared to those from healthy individuals. Hypoxia-induced accumulation of α-smooth muscle actin (αSMA)-positive cells to the PAs is attenuated in p16INK4Afl/fl-Cdh5(PAC)-CreERT2 mice after tamoxifen induction. We have reported that endothelial TWIST1 mediates hypoxia-induced vascular remodeling by increasing PDGFB expression. Transcriptomic analyses of idiopathic pulmonary arterial hypertension (IPAH) patient lung ECs or hypoxia-induced mouse lung ECs reveal the alteration of senescence-related gene expression and interaction with TWIST1. Increases in the levels of PDGFB and TWIST1 in hypoxia-treated mouse lung ECs or IPAH patient lung ECs are attenuated by knocking down p16INK4A expression or treating with senolytic reagents. Knockdown of p16INK4A also suppresses accumulation of αSMA–positive cells to the supplemented ECs in the gel. Exosomes collected from hypoxia-treated mouse lung ECs stimulate SMC DNA synthesis and migration in vitro and in the gel implanted on the mouse lungs, while p16INK4A knockdown in ECs inhibits the effects. These results suggest that endothelial senescence controls αSMA–positive cell proliferation and migration in PH through TWIST1-PDGFB signaling.

2022-10-12 | GSE193272 | GEO

TWIST1

Project description:TWIST1

| PRJNA784600 | ENA

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

Next Generation Sequencing Facilitates Quantitative Analysis of SETD6 Knock-out and stable expression of TWIST1 in Glioblastoma cells

Project description:The goal of this study was to identifiy shared target genes for SETD6 and TWIST1 in Glioblastoma.

2022-07-14 | GSE186047 | GEO

Optimized minimal genome-wide human sgRNA library

Project description:To minimize the human genome-wide CRISPR/Cas9 library size, we established H-mLib which recruited a novel sgRNA design method and applied with dual plasmid based strategy. The performance of the H-mLib was benchmarked to other CRISPR libraries in a proliferation screening conducted in K562 cells. We also identified human core essential genes and cell-type specific essentials genes in K562 and Jurkat cells.

2023-07-18 | GSE223086 | GEO

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