Gene expression profiling of Akt3 over-expressing breast cancer cells after estrogen and tamoxifen treatment
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Jesika Faridi
PROVIDER: E-GEOD-34291 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:LEC rats are considered as interesting model for studying hepatitis and development of hepatocarcinogenesis related to copper accumulation and oxidative stress. LEC rats have a mutation in a gene related to liver copper excretion, the Atp7b gene. As a consequence, this rat strain shows an abnormal copper accumulation in the liver. This is believed to be the origin of the acute hepatitis and the subsequent hepatocellular carcinoma that spontaneously develop in these rats. Here, we present the gene expression profiles of LEC rats at different disease stages. LEC rats were classified as normal 6 weeks old (6w), normal 9 weeks old (9w), slight jaundice and jaundice according to age and disease state. D-penicillamine, a copper chelator agent, blocks both hepatitis and tumor development. D-penicillamine-trated LEC rats were used as control rats for gene expression comparison as they showed neither hepatitis development nor tumor marker expression. Gene expression differences in protein metabolism and tumor marker proteins add to the known oxidative stress and inflammation characterization of the hepatitis process, leading to new insights concerning hepatitis and hepatocarcinogenesis development. Keywords: disease state analysis 6 weeks old LEC rats, 6 rats per group, were sacrified at different hepatitis stages. Biochemical and histological analyses were performed in order to classify the rats into normal, slight jaundice or jaundice groups. D-penicillamine-treated LEC rats (100 mg/kg/day p.o.) were used as control rats since they behave as normal rats. Microarray analysis was performed on liver samples, one replicate per rat, using dyes swap.
2008-04-24 | E-GEOD-7654 | biostudies-arrayexpress
Project description:Voltage gated calcium channels play a central role in regulating the electrical and biochemical properties of neurons and muscle cells. Cells coordinate the expression of voltage gated calcium channels with the expression of other proteins that regulate membrane potential and calcium homeostasis. We report that the C-terminus of CaV 1.2, an L-type calcium channel (LTC) contains a C-terminal fragment that translocates to the nucleus and regulates transcription. This calcium channel associated transcription factor (CCAT) associates with transcriptional co-regulators such as p54nrb/NonO and binds to endogenous promoters. CCAT regulates the expression of gap junctions, sodium calcium exchangers, NMDA receptors, potassium channels and other proteins that regulate neuronal signaling. Electrical activity and developmental processes regulate the nuclear localization of CCAT, suggesting that the CCAT integrates information about the number of LTCs with information about the developmental history and electrical activity of a cell. These findings provide the first evidence that voltage gated calcium channels can directly activate transcription and suggest a novel mechanism linking voltage gated channels to the function and differentiation of excitable cells. Experiment Overall Design: The goal of these experiments was to identify the genes that are regulated by CCAT, a novel transcription factor derived from the C-terminus of CaV1.2. Neuro2A neuroblastoma cells were transfected with the last 503 AA of CaV1.2 which is full length CCAT (CCAT FL) or with the last 280 AA of CaV1.2, a form of CCAT that lacks the transcriptional activation domain (CCAT DTA). The mRNA from either CCAT FL or CCAT DTA expressing cells was hybridized to Agilent mouse genome microarrays along with mRNA from untransfected neuro2A cells (CCAT FL or DTA A series). Subsequent investigation revealed that transfection with the PA1 plasmid by itself increases the expression of some genes. To control for this effect we compared Neuro2A cells transfected with full length CCAT (in PA1) with Neuro2A cells transfectected with PA1 alone (CCAT FL B series). The microarray data was analyzed with the Rossetta Luminator gene expression data analysis system.
2008-06-12 | E-GEOD-4180 | biostudies-arrayexpress
Project description:Microarray analysis is a useful methodology to identify target genes modulated by anticancer drugs. Here, celecoxib effect on gene expression profiles was evaluated in the modified resistant hepatocyte model. Animals subjected to carcinogenic treatment were fed with diet containing 1500 ppm of celecoxib. Two schemes of celecoxib administration were designed. In the progression protocol, celecoxib was administrated between days 18 and 25 post-cancer initiation, a total of 8 celecoxib treatment days, when well established preneoplastic lesions starts to appear. In the initiation protocol, celecoxib was administrated from one week before until 25 days after of cancer initiation, a total of 32 celecoxib treatment days. A rat group was subjected only to the carcinogenic treatment as cancer positive control. Gene expression profiles of all groups were compared to a negative untreated control. The evaluation of gene expression profiles permitted us to identify new target genes that are modulated by celecoxib treatment. A possible mechanism of celecoxib chemoprevention of hepatocarcinogenesis is proposed. 9 weeks old Sprague Dawley rats, 4 rats per group, were subjected to Semple-Roberts' modified hepatocarcinogenesis protocol and sacrificed 25 days post-initiation. In celecoxib-treated groups, celecoxib was administrated mixed in diet at 1500 ppm. Negative and positive cancer progression controls were included to compare gene expression profiles. Microarray analysis was performed on liver samples, one replicate per rat, using dye swap.
2009-07-10 | E-GEOD-12112 | biostudies-arrayexpress
Project description:To identify regions that display DNA copy number alterations in malignant pleural mesothelioma (MPM), we carried out array comparative genomic hybridization (CGH) analysis with 14 MPM cell lines. Regions of genomic aberrations observed in >20% of individuals were 9p21.3, 13q12.11, 16p13, and 22q12.2 of losses. The most frequent alteration was 9p21.3, which include the p16INK4/p14ARF. The loss of 22q12.2 regions include the NF2 was observed in 3 out of 14 cell lines. In 3 cell lines, loss of 13q12.11 region which contains Large Tumor Suppressor, homolog 2 (LATS2) was detected. Human malignant pleural mesothelioma cell lines were profiled on Agilent 244K aCGH arrays according to manufacturer’s instructions. Pooled normal human genomic DNA was used as the reference.
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2010-07-01 | E-GEOD-5088 | biostudies-arrayexpress
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