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Effect of v-erbA on RA-responsive genes in AML12 hepatocytes

ABSTRACT: The v-erbA oncogene belongs to a superfamily of transcription factors called nuclear receptors, which includes the retinoic acid receptors (RARs) responsible for mediating the effects of retinoic acid (RA). Nuclear receptors bind to specific DNA sequences in the promoter region of target genes and v-erbA is known to exert a dominant negative effect on the activity of the RARs. The repressor activity of v-erbA has been linked to the development of hepatocellular carcinoma (HCC) in a mouse model. We have used microarray analysis to identify genes differentially expressed in hepatocytes in culture (AML12 cells) stably transfected with v-erbA and exposed to RA. We have found that v-erbA can affect expression of RA-responsive genes. We have also identified a number of v-erbA-responsive genes that are known to be involved in carcinogenesis and which may play a role in the development of HCC.

ORGANISM(S): Mus musculus

PROVIDER: GSE11703 | GEO | 2008/06/15

SECONDARY ACCESSION(S): PRJNA106115

REPOSITORIES: GEO

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Transcription profiling of mouse AML12 hepatocytes transfected with v-erbA

Project description:The v-erbA oncogene belongs to a superfamily of transcription factors called nuclear receptors, which includes the retinoic acid receptors (RARs) responsible for mediating the effects of retinoic acid (RA). Nuclear receptors bind to specific DNA sequences in the promoter region of target genes and v-erbA is known to exert a dominant negative effect on the activity of the RARs. The repressor activity of v-erbA has been linked to the development of hepatocellular carcinoma (HCC) in a mouse model. We have used microarray analysis to identify genes differentially expressed in hepatocytes in culture (AML12 cells) stably transfected with v-erbA and exposed to RA. We have found that v-erbA can affect expression of RA-responsive genes. We have also identified a number of v-erbA-responsive genes that are known to be involved in carcinogenesis and which may play a role in the development of HCC. Experiment Overall Design: AML12 control cells and v-erbA-transfected AML12 cells were exposed to 1 ÂµM RA for 3h or 24h. Using microarray analysis, we compared gene expression in the presence and absence of v-erbA and identified RA-regulated genes differentially expressed in the presence of v-erbA.

2008-10-20 | E-GEOD-11703 | biostudies-arrayexpress

Effect of v-erbA on T3-responsive genes in AML-12 hepatocytes

Project description:The v-erbA oncogene belongs to a superfamily of transcription factors called nuclear receptors, which includes the thyroid hormone receptors (TRs) responsible for mediating the effects of thyroid hormone (T3). Nuclear receptors bind to specific DNA sequences in the promoter region of target genes and v-erbA is known to exert a dominant negative effect on the activity of the TRs. The repressor activity of v-erbA has been linked to the development of hepatocellular carcinoma (HCC) in a mouse model. We have used microarray analysis to identify genes differentially expressed in hepatocytes in culture (AML12 cells) stably transfected with v-erbA and exposed to T3. We have found that v-erbA can negatively regulate expression of T3-responsive genes known to have a protective function against tumor development. We have also identified a number of v-erbA- (but not T3-) responsive genes that are known to be involved in carcinogenesis and which may play a role in the development of HCC.

2009-06-30 | GSE15458 | GEO

Genome-wide Binding Site Mapping of Retinoic Acid Receptors and Coregulators in Breast Cancer Cells

2009-03-16 | GSE15244 | GEO

Mus musculus

Project description:Effect of v-erbA on RA-responsive genes in AML12 hepatocytes

| PRJNA106115 | ENA

Global analysis of RAR-responsive genes in the Xenopus neurula

Project description:Retinoid signaling is important for patterning the vertebrate hindbrain and midaxial regions. We recently showed that signaling through retinoic acid receptors (RARs) is essential for anteroposterior patterning along the entire body axis. To further investigate the mechanisms through which RARs act, we employed microarray analysis to investigate the effects of modulating RAR activity on target gene expression. We identified 334 upregulated genes (92% of which were validated) including known RA responsive genes, known genes that have never been proposed as RA targets and many hypothetical and unidentified genes (n = 166). 67 validated downregulated genes were identified including known RA responsive genes and anterior marker genes. The expression patterns of selected upregulated genes (n = 45) were examined at neurula stages using whole mount in situ hybridization. We found that most of these genes were expressed in the neural tube and many were expressed in anterior tissues such as neural crest, brain, eye anlagen, and cement gland. Some were expressed in tissues such as notochord, somites, pronephros and blood islands, where retinoic acid (RA) plays established roles in organogenesis. Members of this set of newly identified RAR target genes are likely to play important roles in neural patterning and organogenesis under the control of RAR signaling pathways and their further characterization will expand our understanding of RA signaling during development. Keywords = retinoid Keywords = microarray Keywords = RAR Keywords = neurula Keywords = anteroposterior patterning Keywords = and organogenesis

2010-06-10 | E-GEOD-2295 | biostudies-arrayexpress

Analysis of the transcriptional response to retinoic acid in T47D breast cancer cells with impaired RARA function

Project description:It has been shown that retinoic acid (RA) can both inhibit and promote cancer cell growth, but the basis of this “paradox” is still not clear. The action of RA is mainly mediated by RA receptors (RARs), which classically function as ligand-activated transcription factors. Upon binding to the RA receptor alpha (RARA), RA modulates the transcription of several RA-target genes involved in multiple cellular processes, including cell proliferation. We have found that functional inhibition of RARA transcriptional function by stable expression of a RARA dominant negative (RARA403) converts T47D breast cancer cells from growth-inhibited to growth-promoted by supraphysiological RA (Ren et al., MCB, 2005, PMID:16287870; Somenzi et al., PloS ONE, 2007, PMID:17786207). We hypothesized that RA-induced cell growth requires both the activation of RA-responsive tumor-promoting signalings and lack of activation of RA-responsive tumor suppressor signalings. To identify these signalings, we analyzed the transcriptional response to RA in our model of the “RA paradox” by using gene expression microarrays.

2017-06-01 | GSE57119 | GEO

Global analysis of RAR-responsive genes in the Xenopus neurula

2005-03-05 | GSE2295 | GEO

Relocalization of retinoic acid receptors from non-canonical to canonical spaced binding elements during embryoid body differentiation

Project description:Retinoic Acid Receptors (RARs) bind RA-response elements in regulatory regions of their target genes. While canonical RAREs comprise direct repeats of the consensus 5’-RGKTCA-3’ sequence separated by 1, 2 or 5 nucleotides (DR1, DR2, DR5), we show that shortly after RA treatement of mouse embryoid bodies or F9 cells, RARs occupy a large repertoire of DR0, DR2, DR5, DR8 and IR0 elements. In vitro, RAR-RXR bind these non-canonical spacings with comparable affinities to DR2 and DR5. Most DR8 elements comprise three half sites with DR2 and DR0 spacings. This specific half site organisation constitutes a previously unrecognised, but frequent signature of RAR binding elements and acts as an RARE. At later stages of embryoid body differentiation, RARs relocalise to a restricted repertoire of sites comprising predominantly DR5 elements. Differentiation thus involves genomic relocalisation of RARs, and a switch from DR0 and DR8 at early times to DR5 at later stages. Examination of genomic localisation of RAR in differentiating embryoid bodies.

2012-06-15 | E-GEOD-35599 | biostudies-arrayexpress

Relocalization of retinoic acid receptors from non-canonical to canonical spaced binding elements during embryoid body differentiation

2012-06-15 | GSE35599 | GEO

Genome-wide Binding Site Mapping of Retinoic Acid Receptors and Coregulators in Breast Cancer Cells

Project description:Retinoic acid (RA) triggers growth-suppressive effects in tumor cells and therefore RA and its synthetic analogs have great potential as anti-carcinogenic agents. RA effects are mediated by retinoic acid receptors (RARs), which regulate gene expression in an RA-dependent manner. To define the genetic network regulated by RARs in breast cancer cells, we identified RAR genomic targets using chromatin immunoprecipitation and expression analysis in a model breast cancer cell line MCF-7. Furthermore, we identified genomic binding sites for two putative RAR coregulators FoxA1 and GATA3. Keywords: ChIP-Chip Analysis This series contains ChIP-Chip raw data for four transcription factors (RARA, RARG, FoxA1 and GATA3) in MCF-7 cells. All the experiments are done in triplicates. We mapped the binding sites of RARA, RARG and GATA3 in the bacterial artificial chromosome (BAC) transgenic MCF7 cells in which we tagged the transcription factors with a modified LAP (localization and affinity purification) tag containing green fluorescent protein (GFP). Goat anti-GFP (raised against His-tagged full-length eGFP and affinity-purified with GST-tagged full-length eGFP) was used to perform ChIP experiments in those transgenic lines. To map the binding sites of RARs, MCF7 Cells were hormone-deprived for 3 days and then were treated with 100 nM AM580 (RARA-selective agonist) or 100 nM CD437 (RARG-selective agonist) for 1 hour at 80% confluence. FoxA1 binding sites were mapped using goat anti-FoxA1 antibodies (Abcam: ab5089). Control data include Input from MCF-7 cells. ChIP-Chip experiments with eGFP antibody in wide type MCF-7 cells are used to control eGFP antibody non-specific binding.

2009-03-16 | E-GEOD-15244 | biostudies-arrayexpress

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