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Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch [methylation]

ABSTRACT: Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch [methylation]

PROVIDER: PRJNA525600 | ENA |

REPOSITORIES: ENA

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Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch

Project description:Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch

| PRJNA525597 | ENA

Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch [expression array]

Project description:Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch [expression array]

| PRJNA525351 | ENA

Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch [methylation]

Project description:Distinct subpopulations of neoplastic cells within tumors, including hepatocellular carcinoma (HCC), display pronounced ability to initiate new tumors and induce metastasis. Recent evidence suggests that signals from transforming growth factor beta (TGF-β) may increase the survival of these so called tumor initiating cells leading to poor HCC prognosis. However, how TGF-β establishes and modifies the key features of these cell subpopulations is not fully understood. In the present report we describe the differential DNA methylome of CD133-negative and CD133-expressing liver cancer cells. Next, we show that TGF-β is able to increase the proportion of CD133+ cells in liver cancer cell lines in a way that is stable and persistent across cell division. This process is associated with stable genome-wide changes in DNA methylation that persist through cell division. Differential methylation in response to TGF-β is under-represented at promoter CpG islands and enriched at gene bodies, including a locus in the body of the de novo DNA methyl-transferase DNMT3B gene. Moreover, phenotypic changes induced by TGF-β, including the induction of CD133, are impaired by siRNA silencing of de novo DNA methyl-transferases. Our study reveals a self-perpetuating crosstalk between TGF-β signaling and the DNA methylation machinery, which can be relevant in the establishment of cellular phenotypes. This is the first indication of the ability of TGF-β to induce genome-wide changes in DNA methylation, resulting in a stable change in the proportion of liver cancer cell subpopulations.

2019-03-05 | GSE127828 | GEO

Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch [expression array]

2019-03-05 | GSE127763 | GEO

Dynamic imbalance between cancer cell subpopulations induced by transforming growth factor beta (TGF-β) is associated with a DNA methylome switch.

Project description:BackgroundDistinct subpopulations of neoplastic cells within tumors, including hepatocellular carcinoma (HCC), display pronounced ability to initiate new tumors and induce metastasis. Recent evidence suggests that signals from transforming growth factor beta (TGF-β) may increase the survival of these so called tumor initiating cells leading to poor HCC prognosis. However, how TGF-β establishes and modifies the key features of these cell subpopulations is not fully understood.ResultsIn the present report we describe the differential DNA methylome of CD133-negative and CD133-expressing liver cancer cells. Next, we show that TGF-β is able to increase the proportion of CD133+ cells in liver cancer cell lines in a way that is stable and persistent across cell division. This process is associated with stable genome-wide changes in DNA methylation that persist through cell division. Differential methylation in response to TGF-β is under-represented at promoter CpG islands and enriched at gene bodies, including a locus in the body of the de novo DNA methyl-transferase DNMT3B gene. Moreover, phenotypic changes induced by TGF-β, including the induction of CD133, are impaired by siRNA silencing of de novo DNA methyl-transferases.ConclusionsOur study reveals a self-perpetuating crosstalk between TGF-β signaling and the DNA methylation machinery, which can be relevant in the establishment of cellular phenotypes. This is the first indication of the ability of TGF-β to induce genome-wide changes in DNA methylation, resulting in a stable change in the proportion of liver cancer cell subpopulations.

| S-EPMC4070873 | biostudies-literature

Spleen vs TGF-beta (transforming growth factor-beta) Treated B cell

Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with TGF-beta (transforming growth factor-beta) labeled with Cy5- time course with repeats Keywords: ordered

2003-04-14 | GSE400 | GEO

Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-03-05 | GSE127829 | GEO

Expression data from A549 cells after treatment with flagellin and transforming growth factor beta 1

Project description:We have examined the changes in gene expression aftert reatment of A549 cells, a cultured alveolar epithelial cells, with flagellin and transforming growth factor beta 1. In this dataset, we include the expression data obtained from A549 cells after treatment with purified flagellin or transforming growth factor beta 1 receptor. The analysis indicated that flagellin induced a change in gene expression that was similar to the changes induced by transforming growth factor 1. A549 cells were treated with flagellin or transforming growth factor 1 for 24 h. Total RNA was extracted and reverse transcribed to cDNA. Synthesized cDNA was fragmented and labeled with biotin. The biotinylated cDNA was hybridized to to an Affymetrix GeneChip Array, and probe signal intensities were captured.

2012-10-31 | E-GEOD-38309 | biostudies-arrayexpress

Expression data from A549 cells after treatment with flagellin and transforming growth factor beta 1

2012-10-31 | GSE38309 | GEO

Transforming growth factor beta signaling and decidual development in mice

Project description:Transforming growth factor beta signaling and decidual development in mice

| PRJNA646519 | ENA