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JMJD2B knockdown treatment in normoxia and hypoxia

ABSTRACT: Estrogen receptor alpha plays a critical role in breast cancer and is a major target in endocrine therapy. HIF-1 alpha have been associated with ER alpha and predict a worse outcome. Recent studies indicate that histone demethylase JMJD2B is a HIF-1 alpha target. However, little is known about the biological functions of JMJD2B, especially in breast cancer. To elucidate the mechanism by which JMJD2B reguates gene expression in normoxia and hypoxia, MCF-7 breast cancer cells were depleted forJMJD2B in normoxia and hypoxia. Our results provide insight into JMJD2B regulation of gene expression in breast cancer cells in normoxia and hypoxia. MCF7 cells were subjected to transfection with siRNA controls and two different siRNA oligos against JMJD2B for 24 hours. Cells were treated in normoxia and hypoxia for another 16 hours.

ORGANISM(S): Homo sapiens

SUBMITTER: Francesca Buffa

PROVIDER: E-GEOD-18384 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The histone demethylase JMJD2B is regulated by estrogen receptor alpha and hypoxia, and is a key mediator of estrogen induced growth.

Yang Jun J Jubb Adrian M AM Pike Luke L Buffa Francesca M FM Turley Helen H Baban Dilair D Leek Russell R Gatter Kevin C KC Ragoussis Jiannis J Harris Adrian L AL

Cancer research 20100803 16

Estrogen receptor alpha (ERalpha) plays an important role in breast cancer. Upregulation of HIF-1alpha in ER(alpha)-positive cancers suggests that HIF-1alpha may cooperate with ERalpha to promote breast cancer progression and consequently affect breast cancer treatment. Here, we show the histone demethylase JMJD2B is regulated by both ERalpha and HIF-1alpha, drives breast cancer cell proliferation in normoxia and hypoxia, and epigenetically regulates the expression of cell cycle genes such as CC ...[more]

PMID: 20682797

Similar Datasets

JMJD2B knockdown treatment in normoxia and hypoxia

Project description:Estrogen receptor alpha plays a critical role in breast cancer and is a major target in endocrine therapy. HIF-1 alpha have been associated with ER alpha and predict a worse outcome. Recent studies indicate that histone demethylase JMJD2B is a HIF-1 alpha target. However, little is known about the biological functions of JMJD2B, especially in breast cancer. To elucidate the mechanism by which JMJD2B reguates gene expression in normoxia and hypoxia, MCF-7 breast cancer cells were depleted forJMJD2B in normoxia and hypoxia. Our results provide insight into JMJD2B regulation of gene expression in breast cancer cells in normoxia and hypoxia.

2010-09-01 | GSE18384 | GEO

Identification of JMJD1A and JMJD2B Target Genes in Hypoxic Ovarian Cancer Cells

Project description:The Hypoxia-Inducible Factors induce the expression of the histone demethylases JMJD1A (KDM3A) and JMJD2B (KDM4B), linking the hypoxic tumor microenvironment to epigenetic mechanisms that may foster tumor progression. Using transcript profiling, we have identified genes that are regulated by JMJD1A and JMJD2B in both normoxic and hypoxic conditions in SKOV3ip.1 ovarian cancer cells. This dataset includes expression data obtained from exposing ovarian cancer cells to hypoxia in combination with siRNA-mediated knockdown of the hypoxia-inducible histone demethylases JMJD1A and JMJD2B. These data were used to both identify functional overlap between each histone demethylase, as well as identify effectors of tumor growth mediated by JMJD2B (KDM4B) in normoxia and hypoxia.

2017-03-13 | GSE66894 | GEO

ICI182780 effect on breast cancer cell in hypoxia

Project description:The ER alpha positive breast cancer MCF7 cells were treated with ER alpha antagonist ICI182780 in normoxia and hypoxia. Extracted RNA was subject to microarray analysis. The goal of the experiment is to assess the ICI182780 effect on breast cancer cell in both normoxia and hypoxia.

2015-10-01 | GSE61799 | GEO

Identification of JMJD1A and JMJD2B target genes in hypoxic colon carcinoma cells

Project description:The Hypoxia-Inducible Factors induce the expression of the histone demethylases JMJD1A (KDM3A) and JMJD2B (KDM4B), linking the hypoxic tumor microenvironment to epigenetic mechanisms that may foster tumor progression. This dataset includes expression data obtained from exposing colon carcinoma cells to hypoxia in combination with siRNA-mediated knockdown of the hypoxia-inducible histone demethylases JMJD1A and JMJD2B.

2021-11-03 | GSE166991 | GEO

RNA-seq

Project description:Comprehensive analysis of coding and non -coding transcriptome using ribo-depleted total RNA-seq and poly A selected RNA-seq of MCF-7 cells grown in hypoxia and normoxia. Breast cancer cell line (MCF-7) is cultured in normoxic condition (21% O2) and hypoxic condition (1%O2) for 24 hours. Expression of HIF-1alpha and/or HIF-2alpha subunits was suppressed using siRNAs in hypoxic MCF-7 cells. Total RNA was isolated from both hypoxia and normoxia conditions were subjected for ribosomal depleted stand specific RNA-seq and poly A selected RNA-seq

2014-02-10 | E-MTAB-1994 | biostudies-arrayexpress

Identification of JMJD1A and JMJD2B target genes in renal cell Carcinoma

Project description:The Hypoxia-Inducible Factors induce the expression of the histone demethylases JMJD1A (KDM3A) and JMJD2B (KDM4B), linking the hypoxic tumor microenvironment to epigenetic mechanisms that may foster tumor progression. Using transcript profiling, we have identified genes that are regulated in RCC4 with siRNA-mediated knockdown of JMJD1A and JMJD2B. This dataset includes expression data obtained from renal cell Carcinoma being loss or mutation of the von Hippel-Lindau (VHL) tumor suppressor gene combination with siRNA-mediated knockdown of histone demethylases JMJD1A and JMJD2B.

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Effect of JMJD2B depletion on the ER signaling pathway

2010-12-31 | GSE23445 | GEO

Effect of JMJD2B depletion on the ER signaling pathway

Project description:JMJD2B is expressed in a high proportion of human breast tumors, and the expression levels significantly correlate with estrogen receptor (ER) positivity. To assess the effect of JMJD2B depletion on the ER signaling pathway, we performed genome-wide gene expression analysis using the Affymetrix Human Gene 1.0 ST array. RNA was extracted from steroid-depleted control MCF-7 cells (control E2(-)), control MCF-7 cells treated with E2 (control E2(+)), steroid-depleted JMJD2B-depleted MCF-7 cells (siJ2B E2(-)), and JMJD2B-depleted MCF-7 cells treated with E2 (siJ2B E2(+)).

2010-12-31 | E-GEOD-23445 | biostudies-arrayexpress

Tuning the transcriptional response to hypoxia through HIF prolyl- and asparaginyl-hydroxylase inhibition: Microarray data

Project description:The hypoxia inducible factor (HIF) system orchestrates cellular responses to hypoxia in animals. HIF is an Î±/Î²-heterodimeric transcription factor that regulates the expression of hundreds of genes in a context dependent manner. A hypoxia-sensing component of the HIF system involves oxygen-dependent catalysis by the HIF hydroxylases; in humans there are three HIF prolyl hydroxylases (PHD1-3) and an asparaginyl hydroxylase (FIH). PHD catalysis regulates HIFÎ± levels and FIH catalysis regulates HIF activity. How differences in HIFÎ± hydroxylation status relate to variations in the induction of HIF target gene transcription is unknown. We report studies using small molecule inhibitors of the HIF hydroxylases to investigate the extent to which HIF target gene upregulation is induced by reduced PHD catalysis. The results reveal substantial differences in the role of prolyl- and asparaginyl-hydroxylation in regulating hypoxia responsive genes in cells. Selective PHD inhibitors with different structural scaffolds behave similarly. However, under the tested conditions, a broad-spectrum 2OG dioxygenase inhibitor is a better mimic of the transcriptional response to hypoxia than the selective PHD inhibitors, consistent with an important role for FIH in the hypoxic transcriptional response. Indeed, combined application of selective PHD and FIH inhibitors resulted in transcriptional induction of a subset of genes that were not fully responsive to PHD inhibition alone. Thus, for the therapeutic regulation of HIF target genes, it is important to consider both PHD and FIH activity, and in the case of some sets of target genes, simultaneous inhibition of the PHDs and FIH catalysis may be preferable.

2016-08-31 | E-MTAB-4300 | biostudies-arrayexpress

Identification of hypoxia regulated HIF-1A and HIF-2A specific target genes in Glioblastoma

Project description:HIF-1A and HIF-2A regulate both overlapping and unique target genes in response to hypoxia. In this dataset, we identify specific HIF-1A and HIF-2A target genes in glioblastoma cells. 12 samples were analysed comprising 4 experimental conditions (normoxia scr, hypoxia scr, hypoxia siHIF1, hypoxia siHIF2) in triplicate. We made pairwise comparisons between the averages of each triplicate set to normoxia scr using the Partek suite.

2012-02-25 | E-GEOD-27523 | biostudies-arrayexpress

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