Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The inactive X chromosome is epigenetically unstable and transcriptionally labile in breast cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62907 | GEO | 2015/01/19

SECONDARY ACCESSION(S): PRJNA266311

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The inactive X chromosome is epigenetically unstable and transcriptionally labile in breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-01-19 | E-GEOD-62907 | biostudies-arrayexpress

The inactive X chromosome is epigenetically unstable and transcriptionally labile in breast cancer.

Project description:Disappearance of the Barr body is considered a hallmark of cancer, although whether this corresponds to genetic loss or to epigenetic instability and transcriptional reactivation is unclear. Here we show that breast tumors and cell lines frequently display major epigenetic instability of the inactive X chromosome, with highly abnormal 3D nuclear organization and global perturbations of heterochromatin, including gain of euchromatic marks and aberrant distributions of repressive marks such as H3K27me3 and promoter DNA methylation. Genome-wide profiling of chromatin and transcription reveal modified epigenomic landscapes in cancer cells and a significant degree of aberrant gene activity from the inactive X chromosome, including several genes involved in cancer promotion. We demonstrate that many of these genes are aberrantly reactivated in primary breast tumors, and we further demonstrate that epigenetic instability of the inactive X can lead to perturbed dosage of X-linked factors. Taken together, our study provides the first integrated analysis of the inactive X chromosome in the context of breast cancer and establishes that epigenetic erosion of the inactive X can lead to the disappearance of the Barr body in breast cancer cells. This work offers new insights and opens up the possibility of exploiting the inactive X chromosome as an epigenetic biomarker at the molecular and cytological levels in cancer.

| S-EPMC4381521 | biostudies-literature

The inactive X chromosome is epigenetically unstable and transcriptionally labile in breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

| S-ECPF-GEOD-62907 | biostudies-other

Transcriptionally inactive ATF2 variant drives melanomagenesis

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

2016-05-02 | GSE81014 | GEO

PRC2 represses transcriptionally competent genes on the inactive X-chromosome

Project description:Polycomb repressive complex 2 (PRC2) catalyzes histone H3K27me3, which characterizes many silenced genes including those on the inactive X-chromosome. Here we interrogate the role of core PRC2 protein EED in X-linked gene silencing by assessing allele-specific X-linked gene expression in WT and Eed-/- hybrid mouse trophoblast stem cells (TSCs) harboring a 129/S1-derived maternal X-chromosome and a JF1/Ms-derived paternal X-chromosome. This study generates mRNA-seq data for WT and Eed-/- TSCs, which undergo imprinted inactivation of the paternal X-chromosome. RNA-seq data was mapped allele-specifically to in silico strain-specific maternal and paternal reference genomes, generated based on known single nucleotide polymorphisms. We find that EED loss abrogates H3K27me3 and expression of Xist lncRNA, which is required for X-inactivation, however, despite the absence of H3K27me3 and Xist, only a subset of PRC2 target genes are derepressed in Eed-/- TSCs.

2017-04-07 | GSE84681 | GEO

Stepwise de novo establishment of inactive X chromosome architecture in early development

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

2024-09-10 | GSE206011 | GEO

CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity

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

2020-05-16 | GSE150320 | GEO

A Transcriptionally Inactive ATF2 Variant Drives Melanomagenesis.

Project description:Melanoma is one of the most lethal cutaneous malignancies, characterized by chemoresistance and a striking propensity to metastasize. The transcription factor ATF2 elicits oncogenic activities in melanoma, and its inhibition attenuates melanoma development. Here, we show that expression of a transcriptionally inactive form of Atf2 (Atf2(?8,9)) promotes development of melanoma in mouse models. Atf2(?8,9)-driven tumors show enhanced pigmentation, immune infiltration, and metastatic propensity. Similar to mouse Atf2(?8,9), we have identified a transcriptionally inactive human ATF2 splice variant 5 (ATF2(SV5)) that enhances the growth and migration capacity of cultured melanoma cells and immortalized melanocytes. ATF2(SV5) expression is elevated in human melanoma specimens and is associated with poor prognosis. These findings point to an oncogenic function for ATF2 in melanoma development that appears to be independent of its transcriptional activity.

| S-EPMC4889472 | biostudies-literature