Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA221235 | ENA |
REPOSITORIES: ENA
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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).
2014-08-04 | E-GEOD-51125 | 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.
2014-08-04 | GSE51125 | GEO
Project description:We hypothesized that the expression of many genes are dysregulated during oral cancer carcinogenesis. We examined genome-wide transcript levels in normal mouse tongues and the tongue squamous cell carcinomas induced by 4-NQO. The results will provide important information for the diagnosis, prevention, and treatment of human oral cancers, including tongue cancer. Total RNA obtained from normal tongues (not treated with 4-NQO) and tongue squamous cell carcinomas induced by 4-NQO.
2014-07-01 | E-GEOD-54246 | biostudies-arrayexpress
Project description:We hypothesized that the expression of many genes are dysregulated during oral cancer carcinogenesis. We examined genome-wide transcript levels in normal mouse tongues and the tongue squamous cell carcinomas induced by 4-NQO. The results will provide important information for the diagnosis, prevention, and treatment of human oral cancers, including tongue cancer.
2014-07-01 | GSE54246 | GEO
Project description:Tobacco use and alcohol consumption are two major contributing factors for head and neck squamous cell carcinoma (HNSCC) carcinogenesis. We combined the 4-nitroquinoline-1-oxide (4-NQO) oral carcinogenesis mouse model and the Meadows-Cook alcohol mouse models and performed next generation genome-wide RNA-sequencing of tongues. We determined changes in transcript levels in four groups: 4-NQO followed by ethanol treatment (4-NQO/EtOH), 4-NQO followed by normal drinking water (4-NQO/Untr.), vehicle control followed by ethanol treatment (V.C./EtOH), and vehicle control followed by normal drinking water (V.C./Untr.). We found that the 494 gene transcripts were significantly changed (at least a 2-fold change where p<0.05) in the V.C./EtOH group compared to the V.C./Untr. group. The 4-NQO/Untr. group had 1,808 transcripts significantly changed compared to the V.C./Untr group, while the 4-NQO/EtOH group had 3,606 significantly changed transcripts as compared to the V.C/Untr. group. This study is the first to show that 4-NQO followed by ethanol cause the largest number of changes in transcript levels in the tongue.
2015-10-06 | GSE62125 | GEO
Project description:A better understanding of molecular changes during oral tumorigenesis may help defining new personalized prevention strategies. In order to test this hypothesis, we analyzed whole-genome expression changes in a murine model of oral carcinogenesis, induced by an oral carcinogen (4-NQO) We generated genome-wide expression profiles of microdissected cells from murine tongue at each step of oral tumorigenesis: normal mucosa, hyperplasia, dysplasia and tumor.
2016-12-06 | GSE75421 | GEO
Project description:In order to assess the alteration in lncRNA expression in rat lung carcinogenesis induced by NNK, we determined the lncRNA expression profiles in 3 rat lung tumor samples and matched normal lung tissues and 2 blood samples from the control and NNK treatment group in the 95th week using Arraystar Rat lncRNA Microarray.
2015-05-19 | GSE68967 | GEO
Project description:Thy1 + cells isolated from male F344 rats with Dgalactosamine-induced liver injury were cultured for one week. Bone marrow mesenchymal cells isolated from from the femurs and tibias of a 5-week old male F344 rat. Small hepatocytes (SH) and mature hepatocytes (MH) were isolated from normal livers of 7-week old male F344 rat, Extracellular vesicles (EVs) were separedt from culture media by ultracentrifugation.
2023-04-07 | GSE222517 | GEO
Project description:Global DNA hypomethylation and DNA hypermethylation of promoter regions—including tumor suppressor genes—are frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis. We used microarrays to detail the global programme of gene expression by PGC7/Stella overexpression.
2016-05-13 | GSE68837 | GEO
Project description:Global DNA hypomethylation and DNA hypermethylation of promoter regionsâincluding tumor suppressor genesâare frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis. We used microarrays to detail the global programme of gene expression by PGC7/Stella overexpression. RNA was extracted from NIH3T3 or B16F10 murine cell lines overexpressed PGC7/Stella and was hybridized on Affymetrix microarrays. We compared gene expression levels between control and PGC7/Stella-overexpressed cells. Microarray analysis was performed in NIH3T3 cells including two independent Stella-expressing NIH3T3 clones and a mixture of Stella-expressing NIH3T3 clones and in B16-F10 cells including three independent Stella-expressing B16-F10 clones.
2016-05-13 | E-GEOD-68837 | biostudies-arrayexpress