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Regulation of p21 by TWIST2 contributes to its tumor suppressor function in human acute myeloid leukemia

ABSTRACT: TWIST2 is deregulated in about 1/3 human acute myeloid leukemia (AML) patients partially due to hypermethylation. Overexpression of TWIST2 in various AML cell lines and primary AML cells leads to growth arrest, reduced colony forming cell (CFC) capacity, inhibited cell migration and tumorigenic ability in nude mice, suggesting its tumor suppressor role in AML. To explore the molecular insight of how TWIST2 acts as a tumor suppressor in AML cells, control and TWIST2 expressed THP-1 cells have been analyzed with microarray.

ORGANISM(S): Homo sapiens

PROVIDER: GSE57347 | GEO | 2014/05/07

SECONDARY ACCESSION(S): PRJNA246310

REPOSITORIES: GEO

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Regulation of p21 by TWIST2 contributes to its tumor suppressor function in human acute myeloid leukemia

Project description:TWIST2 is deregulated in about 1/3 human acute myeloid leukemia (AML)M-BM- patients partially due to hypermethylation. Overexpression of TWIST2 in various AML cell lines and primary AML cells leads to growth arrest, reduced colony forming cell (CFC) capacity, inhibited cell migration and tumorigenic ability in nude mice, suggesting its tumor suppressor role in AML. To explore the molecular insight of how TWIST2 acts as a tumor suppressor in AML cells, control and TWIST2 expressed THP-1 cells have been analyzed with microarray. 4 independent biological replicates of control and TWIST2 expressed THP-1 cells have been used for RNA extraction and microarray analysis with Agilent platform.

2014-05-07 | E-GEOD-57347 | biostudies-arrayexpress

Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

Project description:Integrated analysis of genome-wide ChIP-Seq and RNA-Seq data revealed the first dynamic chromatin and transcriptional landscape of Twist2 binding during myogenic differentiation. During differentiation, Twist2 competes with MyoD at shared DNA motifs to direct global gene transcription and repression of the myogenic program. Additionally, TWIST2 shapes the epigenetic landscape to drive chromatin opening at oncogenic loci and chromatin closing at myogenic loci. These epigenetic changes redirect MyoD binding from myogenic genes towards oncogenic, metabolic, and growth genes.

2019-03-08 | GSE127998 | GEO

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [ChIP-seq]

Project description:Sarcomas are derailed in pathways that specify mesenchymal lineages during embryogenesis, causing tumor cells to stall at early stages of differentiation. Among them, rhabdomyosarcoma (RMS) is a pediatric soft tissue sarcoma of skeletal muscle origin. A key feature of RMS is their inability to terminally differentiate despite the high expression of master myogenic regulator MYOD. The bHLH transcription factor TWIST2, which governs mesenchymal stem cell identity and restricts myogenesis, is overexpressed in patient fusion-negative RMS (FN-RMS) tumors. We show that knockdown of TWIST2 enables FN-RMS cells to exit the cell cycle and undergo myogenic differentiation, thereby reducing the growth of FN-RMS xenograft tumors. ChIP-seq analysis revealed that most TWIST2-mediated gene regulation occurs independent of changes in MYOD binding in FN-RMS cells. Instead, TWIST2 controls the deposition of H3K27 acetylation at distal enhancers by interacting with the chromatin remodelers, SMARCA4 and CHD3, to activate growth-related and repress myogenesis-related TWIST2 target genes. Our findings provide new insights into the role of TWIST2 in maintaining an undifferentiated and tumorigenic state of FN-RMS and highlight the clinical potential of reversing the TWIST2-regulated phenotype.

2023-03-20 | GSE207165 | GEO

Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

Project description:Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

| PRJNA526023 | ENA

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [RNA-seq Xenograft]

2023-03-20 | GSE207168 | GEO

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [RNA-seq FN-RMS Cells]

2023-03-20 | GSE207167 | GEO

Effect of Twist2 knockdown on the transcriptional profile of differentiating 3T3-L1 cells

Project description:TWIST2 is a transcription factor heavily involved in proper development. We queried the role of TWIST2 in 3T3-L1 adipogenesis by silencing gene expression using a lentiviral-delivered shRNA and performed RNA-seq at various time points following initiation of differentiation. We found that previously identified TWIST2-target genes increase in transcription, suggesting that TWIST2 acts as a transcriptional repressor in this system.

2022-12-04 | GSE219051 | GEO

Albendazole induces monocytic differentiation in AML cells through modulating KLF4-DPYSL2A axis

Project description:To compare the global gene expressions between KLF4-expressed AML cells and albendazole-treated AML cells, we conducted gene expression arrays in THP-1 cells lentivirally-transduced with doxycycline-inducible KLF4 or in THP-1 cells treated with albendazole in different concentrations. We identified that albendazole induces prominent differentiation in THP-1 cells through up-regulating KLF4 and DPYSL2A expressions. Considering the guaranteed safety and tolerability of albendazole in humans, this drug could easily be repositioned to AML patients once its anti-tumor efficacy is clarified.

2021-03-09 | GSE101784 | GEO

A Twist2-dependent progenitor cell contributes to adult skeletal muscle.

Project description: Not available

| S-EPMC5332283 | biostudies-literature

Kynurenine engages Serotonin Receptor 1b in osteoblasts to reinforce Acute Myeloid Leukemia

Project description:We performed RNAseq analysis of primary human osteoblasts co-cultured with the human THP-1 AML cell-line and, in parallel, RNAseq analysis on the THP-1 AML cells exposed to the human primary osteoblasts.

2020-07-15 | GSE154374 | GEO

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