Project description:Balb/c mice were infected with Leishmania donovani and liver mRNA expression were studied at two months post infection Total RNA was isolated from liver tissue from uninfected and two months infected mouse and whole genome microarray was performed
Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. We carry out paired end , strand specific RNAseq prior to sequencing on Illumina Hiseq 2500 to report on the transcriptional landscape in replicate control mouse livers (n=2), 12 week Phenobarbital exposed livers (n=2)and resulting (35 week PB) liver tumours (n=3).
Project description:A large panel of 81 liver cancer cell models, designated as LIver cancer MOdel REpository (LIMORE) was constructed. These cell lines include 31 public cell lines and 50 new cell models establishend from Chinese liver cancer patients. Whole genome sequencing (WGS), exome sequencing (WES) and RNA sequencing (RNAseq) were performed to obtain the genetic information for these cell lines. These cell lines and associated data provide new models and also a rich resource for liver cancer.
Project description:To examine changes, if any, in the expression of mRNAs in the liver tissue of mice, we have employed whole genome microarray expression profiling as a discovery platform to identify genes responsive to Trichloroethylene (TCE) treatment. In our results, the expression levels of 431 mRNAs were changed after TCE exposure, of which 291 were up-regulated and 140 were down-regulated. Using qPCR, we validated six of the mRNA expression changed genes, viz., Jun, Cdkn1a, Rad51b, Uhrf1, Svil and Ihh. Six B6C3F1 male mice were oral administrated with either corn oil or TCE (dissolved in corn oil, 1000mg/kg b.w per day) for 5 days. The expression changes of mRNAs in TCE exposured mouse liver were screened by whole genome microarray expression profiling and were validated by qPCR.