Project description:Transcriptional profiling of liver cancer associated mesenchymal stem cells comparing normal mesenchymal stem cells from adjacent tumor-free tissues of the same patient 8, Goal was to determine to detect the paracrine trophic factors from liver cancer mesenchymal stem cells. 8 represents liver cancer associated MSCs, N8 represents liver normal MSCs
Project description:Transcriptional profiling of liver cancer associated mesenchymal stem cells comparing normal mesenchymal stem cells from adjacent tumor-free tissues of the same patient 8, Goal was to determine to detect the paracrine trophic factors from liver cancer mesenchymal stem cells. 8 represents liver cancer associated MSCs, N8 represents liver normal MSCs Two-condition experiment, 8 vs. N8 cells. Biological replicates: 1 replicate from the same patient.
Project description:Inflammatory liver disease increases risk of developing liver cancer. The mechanism through which liver disease induces tumorigenesis remains unclear, but is thought to occur via increased mutagenesis. Here, we performed whole-genome sequencing on clonal stem cell organoid lines derived from explanted diseased liver cells from patients with chronic alcohol consumption, non-alcoholic steatohepatitis NASH, and primary sclerosing cholangitis PSC. Surprisingly, we find that these precancerous liver disease conditions do not result in a detectable increased accumulation of mutations, nor altered mutation types in normal stem cells in the liver, which contrasts with typical mutational signatures found in liver tumors. Our findings argue against the idea that liver disease drives tumorigenesis via a direct mechanism of induced mutagenesis, and suggests that the transition from healthy to cancerous liver cells likely occurs through other mechanisms, such as changes to the microenvironment that facilitate the outgrowth of precancerous cells that would normally be suppressed. Increased proliferation of such cells would result in an increase in mutations associated with endogenous mutational processes, which we indeed observed when examining the early stage mutations in a hepatocellular carcinoma.
Project description:To explore the role of small nucleolar RNA (snoRNA) on self-renewal of liver cancer stem cells (CSCs), we isolated liver CSCs (CD133+CD13+) and Non-CSCs (CD133-CD13-) from huamn liver tumor tissues.
Project description:Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goal of this study is to compare the differentially expressed transcriptomes between CD133+ liver cancer stem cells versus CD133- non cancer stem cells by RNA-Seq profiling
