Microarray analysis of gene expression of ovarian cancer cells treated with 1,25-dihydroxyvitamin D3
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE26903 | GEO | 2011/01/28
SECONDARY ACCESSION(S): PRJNA136105
REPOSITORIES: GEO
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Project description:To profile the changes in the pattern of gene expression in human OCa cells induced by 1,25(OH)2D3, OVCAR3 cells were treated with 0.1 pM 1,25(OH)2D3 for 0, 8, 24 and 72 h. The cells were harvested, RNA was extracted, and Affmetrix microarrays were hybridized. OVCAR3 cells were treated with 0.1 pM 1,25(OH)2D3 for 0, 8, 24 and 72 hours. 1,25(OH)2D3 was added at different times to allow the treated cells to be harvested at the same time. Ethanol was included as vehicle controls and all cells were exposed to the same amount of ethanol for the same length of time. Total RNA was extracted using Trizol reagent (Invitrogen) and purified using Qiagen Rneasy kit as recommended by Affymetrix. In the initial set of array analysis with U95 chips, GADD45 was identified to be a VD-induced gene in OVCAR3 cells, which was confirmed by a follow-up study to be a primary target gene. For the array analyses with U133A chips, the response to 1,25(OH)2D3 of the cells used for RNA isolation was ensured by Northern blotting analysis of GADD45. Three independent experiments were performed.
2011-01-28 | E-GEOD-26903 | biostudies-arrayexpress
Project description:Transcriptomic response of mouse mixed neuron-glial cell cultures to 1,25-dihydroxyvitamin D3 6 samples are analysed with three biological replicates in two conditions, control versus 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)
2013-03-25 | E-GEOD-41184 | biostudies-arrayexpress
Project description:The biological effects of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBPβ. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBPβ on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts.
2014-06-02 | GSE51513 | GEO
Project description:The biological effects of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBPβ. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBPβ on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts.
2014-06-02 | GSE51514 | GEO
Project description:The biological effects of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBPβ. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBPβ on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts. RNA was isolated and applied to gene expression microarrays in undifferentiated MC3T3-E1 cells as well as post 15 day osteogenic differentiation MC3T3-E1 cells, which were treated for 24 hours with 10-7M 1,25(OH)2D3. For the vehicle matched samples, please refer to study GSE41955. The samples were completed in biological triplicate.
2014-06-02 | E-GEOD-51514 | biostudies-arrayexpress
Project description:The biological effects of 1?,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBP?. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBP? on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts. 4 transcription factors and 5 histone modifications were examined in undifferentiated MC3T3-E1 cells as well as post 15 day osteogenic differentiation MC3T3-E1 cells, which were treated for 3 hours prior to ChIP assay with ethanol vehicle or with 10-7M 1,25(OH)2D3. For the vehicle matched samples for RUNX2, CEBP beta and histones, please refer to study GSE41955. The samples were completed in biological replicate and examined separately.
2014-06-02 | E-GEOD-51513 | biostudies-arrayexpress
Project description:1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) plays an integral role in calcium homeostasis in higher organisms through its actions in the intestine, kidney and skeleton. Interestingly, while several intestinal genes are known to play a contributory role in calcium homeostasis, the entire caste of key components remains to be identified. To examine this issue, Cyp27b1 null mice on either a normal or a high calcium/phosphate-containing rescue diet were treated with either vehicle or 1,25(OH)2D3 and evaluated 6h later. RNA samples from duodena were then subjected to RNA-seq analysis and the data analyzed bioinformatically. 1,25(OH)2D3 altered expression of large collections of genes raised under either dietary condition. 45 genes were found common to both 1,25(OH)2D3-treated groups, and were comprised of genes previously linked to intestinal calcium uptake including S100g, Trpv6, Atp2b1 and Cldn2 as well as others. An additional distinct network of 56 genes was regulated exclusively by diet. This study revealed a global network of genes in the intestine that both represent direct targets of vitamin D action in mice and are involved in calcium absorption.
2015-06-03 | GSE69170 | GEO
Project description:1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) plays an integral role in calcium homeostasis in higher organisms through its actions in the intestine, kidney and skeleton. Interestingly, while several intestinal genes are known to play a contributory role in calcium homeostasis, the entire caste of key components remains to be identified. To examine the vitamin D receptor (VDR) cistrome in this issue, we conducted a ChIP-seq analysis of binding sites for the VDR across the proximal intestine in vitamin D-sufficient normal mice treated with vehicle or 1,25(OH)2D3. The residual VDR cistrome was comprised of 4617 sites which was increased almost 4-fold following hormone treatment. Interestingly, the majority of the genes regulated by 1,25(OH)2D3 in each diet group as well as those found in common in both groups contained frequent VDR sites that likely regulated their expression. This study revealed a global VDR cistrome regulating a network of genes in the intestine that both represent direct targets of vitamin D action in mice and are involved in calcium absorption.
2015-06-03 | GSE69179 | GEO
Project description:A major goal in prostate stem cell biology is to identify genes, pathways, or networks that control self-renewal and multilineage differentiation. We hypothesize that 1,25 dihydroxyvitamin D3 can induce differentiation of prostatic progenitor/stem cells, thus serving as an in vitro model with which to study the molecular mechanisms of stem cell differentiation by 1,25 dihydroxyvitamin D3. 1,25 dihydroxyvitamin D3 elicits its effects primarily through transcriptional regulation of genes, so microarray studies were used to gain insight into the cellular response to 1,25 dihydroxyvitamin D3. We used microarrays to detail the global gene expression changes that occur upon 1,25 dihydroxyvitamin D3 treatment of prostatic progenitor/stem cells. Adult mouse prostate progenitor/stem cells were plated at 1 x 10^5 cells per 10 cm culture dish and grown to 70% confluency before treatment with vehicle (0.1% ethanol) or 100 nM 1,25(OH)2D3 in cell culture media (n = 3 or 4). Cells were treated with control or experimental media for 6 hrs or 48 hrs before RNA isolation. The RNA from 6 hrs and 48 hrs was used to probe Affymetrix 430A oligonucleotide arrays (GPL339).
2011-06-22 | E-GEOD-18993 | biostudies-arrayexpress
Project description:1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) plays an integral role in calcium homeostasis in higher organisms through its actions in the intestine, kidney and skeleton. Interestingly, while several intestinal genes are known to play a contributory role in calcium homeostasis, the entire caste of key components remains to be identified. To examine the vitamin D receptor (VDR) cistrome in this issue, we conducted a ChIP-seq analysis of binding sites for the VDR across the proximal intestine in vitamin D-sufficient normal mice treated with vehicle or 1,25(OH)2D3. The residual VDR cistrome was comprised of 4617 sites which was increased almost 4-fold following hormone treatment. Interestingly, the majority of the genes regulated by 1,25(OH)2D3 in each diet group as well as those found in common in both groups contained frequent VDR sites that likely regulated their expression. This study revealed a global VDR cistrome regulating a network of genes in the intestine that both represent direct targets of vitamin D action in mice and are involved in calcium absorption. Wildtype mice were fed a standard rodent chow diet (Harlan Teklad, #5008). At 8 weeks of age, 3 mice were treated with 1,25(OH)2D3 (10 ng/g bw) or vehicle control and the proximal half of the small intestine (duodenum and jejunum) was collected 1 h later.
2015-06-03 | E-GEOD-69179 | biostudies-arrayexpress