Project description:the Hepa1-6-bearing C57 BL/6 mouse model was utilized to explore the therapeutic efficacy of Ganoderma lucidum extract (GLE), documenting that it could effectively inhibit tumor growth. Furthermore, the microRNA (miRNA) profiles of GLE-treated and untreated mice were detected, and 25 differential expressed (DE) miRNAs were determined, including 24 up-expressed and one down-expressed miRNAs., documenting that it could effectively inhibit tumor growth. Furthermore, the microRNA (miRNA profiles of GLE-treated and untreated mice were detected, and 25 differential expressed (DE miRNAs were determined, including 24 up-expressed and one down-expressed miRNAs.
Project description:Hepa1-6-bearing C57BL/6 mouse model was established to evaluate the therapeutic efficacy of Ganoderma lucidum extract (GLE) in HCC. The GLE treated and untreated mice were used for transcriptioanl profiles detection, and 126 differentially expressed lncRNAs and 558 DE mRNAs were identified, respectively. The bioinformatics analysis shows that the GLE could suppress the growth and proliferation of HCC by PI3K/Akt/mTOR and MAPK signaling pathway, and also could induce apoptosis of tumor cell by mitochondrial and death receptor pathway.
Project description:Purpose: investigating paracrine effects of mono- and/or co-cultured LSEC and Hepa1-6 Method: mRNA profiles of mono- and co-cultured LSEC and Hepa1-6 were generated by deep sequencing. Results: The RNA-seq data confirmed that extracellular matrix-encoding genes were up-regulated by co-cultured LSEC with Hepa1-6.
Project description:To find out which miRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed miRNA microarray as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The miRNA microarray experiments were performed together.
Project description:Liver cancer has a high mortality rate. Chronic inflammation is one of the leading causes of hepatocellular carcinoma. Recent studies suggested high levels of trimethylamine N-oxide (TMAO) may correlate with increased risk of inflammatory-induced liver cancer. However, the mechanisms by which TMAO promotes liver cancer remain elusive. Here, we established a model of inflammatory-induced liver cancer by treating Hepa1-6 cells with TNF-α. TMAO synergistically increased the proliferation, migration and invasion of Hepa1-6 cells in the presence of TNF-α. We conducted bulk RNA-Seq of the TMAO-treated cell model of inflammatory Hepatocellular carcinoma (HCC)
Project description:Unravelling molecular defects resulting from the missense mutation in TBL1XR1 using targeted mutant mice bearing the Tbl1xr1 Y446C/Y446C mutation. These mice used as an animal model of Pierpont syndrome have disturbed hearing and subtle changes in fat metabolism. RNA seq of white adipose tissue has been performed to establish the transcriptome.