Project description:To explore the mechanism of PTEN function, we determined the gene expression profiles of RBE and HCCC-9810 cells infected with PTEN adenovirus. Pathway and GO-term enrichment analyses suggested that the proteasome and ubiquitin-mediated proteolysis pathways were specifically affected in HCCC-9810 cells
Project description:Gene expression of hepatocyt-specific knockout of Pten and of Pten and Tgfbr2 in mice as a model for human cholangiocarcinoma was determined Affymetrix Mouse 1.0ST chips were used to measure gene expression Gene expression of the following mouse livers were characterized A. WT (n=3). B. Pten-/- (n=4). C. Pten-/- Tgfbr2-/- (n=4).
Project description:Intrahepatic cholangiocarcinoma (ICC) is known to have a poor prognosis among primary liver cancers. We created a mouse model of cholangiocarcinogenesis by specifically deleting Pten and Traf3 in the liver. RNA sequence was performed with RNA extracted from the liver of mice lacking liver-specific Pten and Traf3.
Project description:Gene expression of hepatocyt-specific knockout of Pten and of Pten and Tgfbr2 in mice as a model for human cholangiocarcinoma was determined Affymetrix Mouse 1.0ST chips were used to measure gene expression
Project description:Background: PTEN loss contributes to the development of many cancers and is associated with both hepatocellular carcinoma and cholangiocarcinoma. The pathogenesis of these malignancies is unclear, but they are speculated to arise from common cellular origins. We explored the influence of secondary effects, like hypoxia signaling, through co-deletion of Pten and Vhl in a murine model.Methods: We used a CreER-linked keratin 18 mouse model to conditionally delete Pten, Vhl or both, evaluating the resultant tumors by histology and gene expression microarray. A cohort of human cholangiocarcinoma samples was evaluated for relationships between HIF-1a expression and clinical outcomes.Results: Both Pten deletion genotypes developed liver tumors, but with differing phenotypes. Pten deletion alone led to large, invasive tumors with widespread hepatosteatosis. Co-deletion of Pten and Vhl resulted in low tumor burden and reduced steatosis. Microarray analysis divided mouse tumors’ respective genotypes by gene expression. This gene expression profile grouped a human tumor cohort according to histologic type with the Pten deletion signature aligning with hepatocellular carcinoma, whereas the Pten; Vhl deletion signature associated with cholangiocarcinomas. In a human cholangiocarcinoma cohort, we observed correlation between HIF-1a expression and overall survival.Conclusions: Pten deletion leads to tumor formation and steatosis in mouse livers. Co-deletion of Vhl and Pten resulted in lower tumor burden with gene expression profiling suggesting a switch from hepatocellular expression features to an expression profile more consistent with cholangiocarinoma. A possible relation between HIF-1a expression and increased overall survival in human cholangiocarcinoma suggests that hypoxia signaling influences tumor phenotype. reference x sample
Project description:Intrahepatic cholangiocarcinoma (ICC) is known to have a poor prognosis among primary liver cancers. We created a mouse model of cholangiocarcinogenesis by specifically deleting Pten and Traf3 in the liver. single cell RNA sequence was performed with RNA extracted from the liver of mice lacking liver-specific Pten and Traf3.
Project description:Intrahepatic cholangiocarcinoma (ICC) is known to have a poor prognosis among primary liver cancers. We created a vitro model of cholangiocarcinogenesis using HepG2 with specifically knockdown of Pten and Traf3. RNA sequence was performed with RNA extracted from the liver of mice lacking liver-specific Pten and Traf3.
Project description:The aim of the study was to characterize the transcriptional profiles of two cholangiocarcinoma cell lines (HuCCT1 and Huh28) after a treatment with Transforming Growth Factor beta (TGF-beta).
Project description:To investigate the molecular mechanism of EBF1 in cholangiocarcinoma cell line, RNA sequencing analysis was performed to investigate the differential gene expression profiles between EBF1 overexpression group and control group in KKU-213A cells.