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The Breast Cancer Susceptibility Gene TOX3 Promotes Estrogen Synthesis: An RNA-sequencing and Network Study

ABSTRACT: The Breast Cancer Susceptibility Gene TOX3 Promotes Estrogen Synthesis: An RNA-sequencing and Network Study

PROVIDER: PRJNA677925 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13041589_1.fastq.gz	Fastqsanger.gz
	SRR13041589_2.fastq.gz	Fastqsanger.gz
	SRR13041590_1.fastq.gz	Fastqsanger.gz
	SRR13041590_2.fastq.gz	Fastqsanger.gz
	SRR13041591_1.fastq.gz	Fastqsanger.gz

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The Breast Cancer Susceptibility Gene TOX3 Promotes Estrogen Synthesis: An RNA-sequencing and Network Study

Project description:We aimed to explore the effect of the breast cancer susceptibility gene TOX3 on estrogen synthesis from the perspective of estrogen production, in an attempt to link abnormalities in hormone production with the development of breast cancer. After overexpression of TOX3, several crucial key genes and pathways that contribute to estrogen production were upregulated. Forced expression of TOX3 also promotes proliferation and inhibits apoptosis of granulosa cells. These findings discuss the possible impact of susceptibility genes and steroid hormones on breast cancer from the perspective of extra-mammary tissues such as those in the ovary, thus providing new insights for early prevention and treatment of breast cancer.

2021-02-04 | GSE161341 | GEO

TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1 [ChIP-seq]

Project description:Purpose: The goals of this study are to explore role of Tox3 in glucose homeostasis Methods: Tox3-activation was generated by adenovirus from Genechem.Successful activation of Tox3 was determined by mRNA and protein expression.

2024-01-22 | GSE228791 | GEO

TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1 [RNA-seq]

2024-01-22 | GSE228790 | GEO

TOX3 is Expressed in Mammary ER Positive Epithelial Cells and Regulates a Subset of ER Target Genes in a Ligand-Independent Manner in Luminal Breast Cancer

Project description:To assess how the TOX3 nuclear protein can modulate gene expression in luminal epithelial cells, MCF7 cells were transfected with a TOX3 expression vector or vector control. In both instances, GFP was coexpressed, allowing isolation of transfected cells by flow cytometry before transcriptome analysis. Experiments were carried out under estrogen depleted conditions, and cells isolated 48 hours after transfection.

2014-12-01 | GSE57856 | GEO

<i>TOX3</i> Promotes Ovarian Estrogen Synthesis: An RNA-Sequencing and Network Study.

Project description:BackgroundWomen who undergo chronic exposure to excessive estrogen are at a high risk of developing breast cancer. TOX3 has been reported to be highly expressed in breast tumors and is closely related to estrogen receptors. However, the effect of TOX3 on estrogen synthesis remains poorly understood.MethodsUsing lentiviruses as a vector, we stably overexpressed TOX3 in the ovarian granulosa cell line KGN, the cells where estradiol is primarily produced, to investigate its role in estrogen production as well as cell viability and apoptosis. RNA-Sequencing was applied to uncover the global gene expression upon TOX3 overexpression.ResultsWe observed an increased level of cell viability and a reduced cell apoptosis rate after TOX3 overexpression, and the level of estradiol in the cell culture supernatant also increased significantly. Gene set enrichment analysis of the transcriptome showed that the ovarian steroidogenesis pathway was significantly enriched. Similarly, pathway mapping using the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analyses also showed that TOX3 overexpression affects the ovarian steroidogenesis pathway. Further experiments showed that upregulated FSHR, CYP19A1, and BMP6 accounted for the enhanced estrogen synthesis.ConclusionOur study demonstrated that TOX3 quantitatively and qualitatively stimulates estrogen synthesis by enhancing estrogen signaling pathway-related gene expression in ovarian granulosa cells. These findings suggest that TOX3 may play a vital role in the pathogenesis of breast cancer.

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Inflammation and tumor susceptibility in skin cancer

Project description:This SuperSeries is composed of the following subset Series: GSE12248: Genetic architecture of murine skin inflammation and tumor susceptibility GSE21247: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (carcinomas) GSE21263: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (papillomas) GSE26273: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (aCGH) Refer to individual Series

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Mapping of Three Genetic Determinants of Susceptibility to Estrogen-Induced Mammary Cancer within the Emca8 Locus on Rat Chromosome 5

Project description:We are using the ACI rat model of 17beta-estradiol induced mammary cancer to define the mechanisms through which estrogens contribute to breast cancer development; identify and functionally characterize the genetic variants that determine susceptibility; and define the hormone-gene-environment interactions that influence development of mammary cancer in this physiologically relevant rat model. Female ACI rats are uniquely susceptible to development of mammary cancer when treated continuously with physiologic levels of 17beta-estradiol. Induction of mammary cancer in female ACI rats occurs through a mechanism that is largely dependent upon estrogen receptor-alpha. Interval mapping analyses of progeny generated in intercrosses between susceptible ACI rats and resistant Brown Norway (BN) rats revealed seven quantitative trait loci (QTL), designated Emca3 (Estrogen-induced mammary cancer) through Emca9, each of which harbors one or more genetic determinants of mammary cancer susceptibility. Genes that reside within Emca8 on RNO5 and were differentially expressed between 17beta-estradiol treated ACI and ACI.BN-Emca8 congenic rats were identified as Emca8 candidates.

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Estrogen responsive transcriptome of estrogen receptor positive normal human breast cells in 3D cultures

Project description:Understanding how differentiation, microenvironment, and hormonal milieu influence human breast cell susceptibility to malignant transformation will require the use of physiologically relevant in vitro systems. We developed a 3D culture model that enables the propagation of normal estrogen receptor alpha (ER)+ cells. The purpose of this experiment was to assess ER functionality and compare estrogen-induced transcripts among samples and systems.

2018-06-15 | GSE115112 | GEO

TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1

Project description:TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1

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Mapping of Three Genetic Determinants of Susceptibility to Estrogen-Induced Mammary Cancer within the Emca8 Locus on Rat Chromosome 5

2013-02-08 | E-GEOD-39788 | biostudies-arrayexpress