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Expression data with either EglN2 or control knockdown in T47D cells

ABSTRACT: In order to perform integrated analysis for EglN2 ChIP-Seq and microarray to identify EglN2 direct target genes, we performed the microarray analysis for T47D breast cancer cells with either control or EglN2 siRNA followed by hypoxia+DMOG treatment T47D cells were transfected with either control or EglN2 siRNA in duplicate with RNAi max. 36 hours following transfection, cells were treated with hypoxia (1%) and DMOG (1 mM) for 16 hours. Following treatment, total RNA was extracted using Rnaeasy kit from Qiagen.

ORGANISM(S): Homo sapiens

SUBMITTER: Qing Zhang

PROVIDER: E-GEOD-59936 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:We report the comprehensive genome-wide binding peaks for key factors inovled in oxygen sensing pathways, such as HIF1α, HIF1β and EglN2. In addition, we also report the genome-wide binding peaks for NRF1 in breast cancer cells We conducted HA-EglN2, HIF1α, HIF1β (ARNT) or NRF1 ChIP-Seq in the T47D cell line that overexpresses HA-EglN2 in the presence of hypoxia (1%) and DMOG treatment. T47D parental cells treated with the same condition followed by HA ChIP-seq served as the control to filter non-specific binding.

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

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Expression data with either EglN2 or control knockdown in T47D cells

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2014-07-31 | GSE59936 | GEO

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Study of SPEN overexpression in T47D cells. (2)

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Project description:Split Ends (SPEN) is a transcriptional coregulator that have formerly identified as a tumour suppressor gene in ER-positive breast cancers. However, ER-positive breast cancers are diagnosed at similar frequencies in pre- and post-menopausal women who show significantly different circulating hormone levels. This therefore raises the possibility that SPEN functions under hormone-depleted settings may contrast with its roles in the presence of hormones. We therefore attempted to explore the cellular functions regulated by SPEN under hormone-depleted settings using a previously established model with T47D cells stably transfected with a control vector (non-target) or SPEN-expressing vector. In particular, we attempted to investigate the hormone-independent transcriptional program regulated by SPEN in breast cancer. To achieve this, we have treated previously established T47D cells stably transfected with a control vector (non-target) or SPEN-expressing vector. These cells were allowed to grow in hormone-depleted conditions for 4 days. To minimize external biases introduced by hormone depletion or any transcriptional contribution from the estrogen receptor (ER), we also performed gene expression profiling analyses on the same cells but stimulated with an estrogen receptor (ER) agonist (Estradiol) or antagonist (Tamoxifen).

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