Expression data from rats esophagi
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE60439 | GEO | 2014/08/16
SECONDARY ACCESSION(S): PRJNA258261
REPOSITORIES: GEO
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Project description:This microarray study was performed to investigate the molecular events in esophageal SCC carcinogenesis in NMBA induced rat esophageal SCC models. Rats were housed 3 per cage under standard conditions: 20 ± 2ºC, 50±10% relative humidity, and 12 hours light/dark cycles. After two weeks of acclimation to the animal facility, the rats were administered s.c. injections of 0.2 ml of either NMBA (0.3 mg/kg body weight) or a 1:4 mixture of dimethyl sulfoxide (DMSO):H2O (the solvent for NMBA) 3 times per week for 5 weeks.
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Project description:Transcriptome analysis of RNA samples from riboflavin deficiency combined with NMBA-induced rat esophageal intraepithelial neoplasia tissues. Epidemiological studies suggest that dietary riboflavin deficiency and environmental exposure to N-nitrosomethylbenzylamine (NMBA) are common in China's high incidence area of esophageal cancer. Riboflavin deficiency has been documented as an important risk factor for esophageal cancer. In this study, we established a F344 rat esophageal tumor model that combines dietary riboflavin deficiency with exposure to NMBA. The results showed that riboflavin deficiency combined with NMBA (R0N+) enhanced the incidence of esophageal intraepithelial neoplasia, including in situ carcinoma, whereas normal levels of riboflavin combined with NMBA (RcN+) mainly induced the occurrence of esophageal benign hyperplasia and small amount of esophageal intraepithelial neoplasia. Oxidative DNA damage (8-OHdG) and DNA double-strand breaks (p-γH2AX) in R0N+ rats were higher than that in RcN+ rats. The aim of the present study is to analyze the mechanism of riboflavin deficiency-induced tumorigenesis. So, we used Affymetrix Clariom D(also known as Rat Transcriptome Array 1.0) to identify genes that were differentially expressed upon R0N+ esophageal intraepithelial neoplasia tissues.
2018-02-28 | GSE111207 | GEO
Project description:To date, there is little information on early molecular events in the development of N-nitrosomethylbenzylamine (NMBA) induced esophageal tumorigenesis and of the effects of chemopreventive agents on these events. In this study, we identified genes in rat esophagus that were differentially expressed in response to short–term NMBA-treatment and modulated by co-treatment with phenethylisothiocyanate (PEITC). Rats were fed AIN-76A diet or AIN-76A diet containing PEITC for three weeks. During the third week of dietary treatment, they were administered three s.c. doses of NMBA (0.5 mg/kg b.w.). Rats were sacrificed 24 h after the last treatment, esophagi excised and processed for histological grading, microarray and real-time PCR analysis. Our histopathological data showed that treatment of rats with PEITC had protective effect on NMBA-induced preneoplastic lesions in the rat esophagus. We identified 2261 genes that were differentially expressed in the NMBA-treated vs. control esophagi and 1936 genes in the NMBA+PEITC- vs. NMBA-treated esophagi. The intersection of these two sets resulted in the identification of 1323 genes in NMBA-treated esophagus that were modulated by PEITC to near-normal levels of expression. The measured changes in the expression levels of 10 selected genes were validated using real-time PCR. Principle components analysis (PCA) was applied to all twelve microarrays in the study, which suggested that in terms of global gene expression, PEITC treatment had a genome-wide modulating effect on NMBA-induced gene expression. Samples obtained from animals treated with PEITC alone or co-treated with NMBA were more similar to controls than they were to NMBA treatment alone. Keywords: Toxicogenomics,reference design
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Project description:Weaning male Sprague-Dawley rats were divided into 2 dietary groups to form the Zn-deficient (ZD) and Zn-sufficient (ZS) groups. After 5 weeks, the animals received intragastrically, their 1st N-nitrosomethylbenzylamine dose (NMBA, an esophagus carcinogen) at 2 mg/kg body weight. Immediately after NMBA treatment, half of the ZD rats were switched to a ZS diet to form the Zn-replenished (ZR) group, the other half of ZD rats and ZS rats continued on their respective diets. Five weeks after the 1st NMBA dose, 8 ZD, 8 ZR, and 8 ZS rats were sacrificed gene expression profiling and related studies. The remaining rats received their 2nd and 3rd NMBA dose at 6 weeks and 12 weeks after the 1st NMBA dose. At 15 weeks (endpoint) after the 1st NMBA dose, all animals were sacrificed for tumor incidence analysis and gene expression profiling studies. In this study, ZD rats documented a significantly higher tumorigenic outcome than control ZS rats (tumor incidence, ZD vs ZS: 100% vs 16.6%; tumor multiplicity, 11 ± 3.8 vs 0.5 ± 0.3, P<0.001). Replenishing zinc after the first NMBA dose led to a significantly reduced tumor incidence and multiplicity in ZR vs ZD rats (incidence, 28.9% vs 100%; multiplicity, 0.6 ± 0.4 vs 11 ± 3.8, P<0.001). Expression profiling of esophageal epithelia from NMBA-treated ZD, ZR, and control ZS rats (n=4/group) was performed at 5 weeks and at 15 weeks after the 1st carcinogen dose, using Rat Genome 230 2.0 GeneChip (Affymetrix, Santa Clara, CA)
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Project description:To date, there is little information on early molecular events in the development of N-nitrosomethylbenzylamine (NMBA) induced esophageal tumorigenesis and of the effects of chemopreventive agents on these events. In this study, we identified genes in rat esophagus that were differentially expressed in response to shortâ??term NMBA-treatment and modulated by co-treatment with phenethylisothiocyanate (PEITC). Rats were fed AIN-76A diet or AIN-76A diet containing PEITC for three weeks. During the third week of dietary treatment, they were administered three s.c. doses of NMBA (0.5 mg/kg b.w.). Rats were sacrificed 24 h after the last treatment, esophagi excised and processed for histological grading, microarray and real-time PCR analysis. Our histopathological data showed that treatment of rats with PEITC had protective effect on NMBA-induced preneoplastic lesions in the rat esophagus. We identified 2261 genes that were differentially expressed in the NMBA-treated vs. control esophagi and 1936 genes in the NMBA+PEITC- vs. NMBA-treated esophagi. The intersection of these two sets resulted in the identification of 1323 genes in NMBA-treated esophagus that were modulated by PEITC to near-normal levels of expression. The measured changes in the expression levels of 10 selected genes were validated using real-time PCR. Principle components analysis (PCA) was applied to all twelve microarrays in the study, which suggested that in terms of global gene expression, PEITC treatment had a genome-wide modulating effect on NMBA-induced gene expression. Samples obtained from animals treated with PEITC alone or co-treated with NMBA were more similar to controls than they were to NMBA treatment alone. Experiment Overall Design: For each treatment we used a pooling strategy to enable the inclusion of samples from numerous animals. Three replicate microarrays were completed for each of the four treatments (control, PEITC, NMBA and NMBA+PEITC) for a total of twelve microarrays. Each microarray was hybridized using a pooled RNA sample, and each pool was created from equal amounts of total RNA from two or three independent RNA samples, representing individual animals. Each of these samples was obtained from a different animal, and no sample was included in more than one pool. In total, samples from nine animals per group were pooled for control, NMBA, PEITC and NMBA+PEITC microarrays. To facilitate comparisons of gene expression across all treatments, we utilized a reference design in which each microarray was co-hybridized with a common reference sample labeled with Cy3, and RNA from the treatment pool was labeled with Cy5. Stratageneâ??s Universal Rat reference RNA (Stratagene, La Jolla, CA) was used as the common reference in all microarrays.
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Project description:Lineage-survival oncogenes are targeted by gene amplification in cancers arising from the tissues where these genes play a role in normal development. Here we show that the transcription factor SOX2—previously known to be mutated in hereditary human esophageal malformations, to be necessary for normal esophageal squamous development, to promote proliferation of basal tracheal cells and to co-operate in induction of pluripotent stem cells -- acts as an amplified oncogene in squamous cell carcinomas (SCC) of the lung and esophagus. We identified SOX2 at a peak of genomic amplification on chromosome 3q26.33 in SCCs of both the lung and esophagus but did not find it to be significantly amplified in adenocarcinomas from these tissues. Tumors with SOX2 amplification showed higher SOX2 mRNA expression, and suppression of SOX2 by RNAi in lung and esophageal SCC cell lines revealed that SOX2 expression is required for proliferation and anchorage-independent growth. Furthermore, ectopic expression of SOX2 cooperated with FOXE1 or FGFR2 to transform immortalized tracheobronchial epithelial cells. SOX2-driven tumors showed expression of markers of both squamous differentiation and pluripotency. These observations identify SOX2 as a novel lineage survival oncogene in lung and esophageal SCC and suggest novel connections between development, pluripotency and carcinogenesis.
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2010-07-09 | E-GEOD-13937 | biostudies-arrayexpress
Project description:Esophageal squamous cell carcinoma (SCC) is frequently diagnosed at advanced stage and associated with poor prognosis. This study aimed to identify differentially expressed genes for further evaluated as biomarkers for predicting survival of the patients. Five paired of cancerous and normal tissues from esophageal SCC patients were subjected to cDNA microarray analysis and one of these differentially expressed genes, NEK6, was further verified in esophageal SCC tissues. The data showed 444 up-regulated genes and 918 down-regulated genes in tumor tissues (2 folds as a cut-off value). qRT-PCR data showed that 20 of 30 (66.7%) increased levels of NEK6 mRNA in cancerous tissues compared to that of distant normal tissues, while immunohistochemical data showed that 49/94 (52.13%) of the archived esophageal SCC tissues expressed higher levels of NEK6 than that of normal tissues. NEK6 expression was associated with depth of tumor invasion (P=0.005), lymph node metastasis (P=0.018), and advanced clinical tumor stages (P=0.004) of these 94 patients. Kaplan Meier curve showed that the overall survival of NEK6-positive patients was much lower than those of NEK6-negative patients (P<0.001). The median survival of NEK6-positive patients was 23 months, whereas the median survival of NEK6-negative patients was 64 months. The cumulative 5-year survival rate of NEK6-positive patients was 14.3% (7/49), whereas the rate of NEK6-negative patients was 64.4% (29/45). Multivariate analysis showed that N classification (P=0.002) and NEK6 expression (P<0.001) were independent predictors for esophageal SCC patients. These data demonstrated that NEK6 expression may serve as an independent prognostic indicator for patients with esophageal SCC. Gene expression in five paired of cancerous and normal tissues from esophageal SCC patients were measured using Human Genome 4x44K v2 Microarray.
2013-09-30 | E-GEOD-45168 | biostudies-arrayexpress
Project description:The 4-NQO induced rat tongue carcinogenesis model presenting considerable histologic and molecular similarity to oral cancers commonly seen in humans is very useful for investigating oral carcinogenesis. In order to understand the molecular basis of oral carcinogenesis and identify gene biomarkers and potential chemopreventive targets for future studies, we characterized the molecular changes in oral squamous cell carcinoma (SCC) samples generated from this model system using F344 rats by performing gene expression microarray and methylation analysis of selected genes. Microarray studies identified 1735 genes to be upregulated by at least 2 fold (p<0.05, n=11) and 1803 genes to be downregulated by at least 50% (p<0.05, n=11) in SCC in comparison to the adjacent normal tissues and 28 KEGG pathways to be altered in SCC (p<0.01). Among the altered genes, keratins and keratin associated proteins were found to be differentially regulated and the keratin profile appeared to an important biomarker for oral SCC. PTGS2 and PTGS2 relevant genes, which are potential targets of chemoprevention and therapy, were also found to be upregulated in SCC and confirmed by qRT-PCR. The upregulation of PTGS2 appeared to correlate with hypomethylation of its proximal promoter. Methylation analysis of other selected genes showed that the first exon of APC2 was methylated in normal tissues, and the methylation level increased moderately in SCC samples (p<0.01, n=8). These results demonstrate that 4-NQO induced tongue carcinogenesis in F344 rats is accompanied by alteration of multiple gene expression, hypomethylation of PTGS2 and increased methylation of APC2. Gene expression in untreated normal vs.4-NQO induced tongue tumors in F344 rats (n=11).
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