Project description:To demonstrate CD133+CD44+ and CD133+CD44- subpopulations of hepatocellular carcinoma as distinct subgroups, we have employed whole genome microarray expression profiling as a discovery platform to reveal the gene profiles of different subgroups and identify genes responsible for the enhanced metastatic potentials of CD133+CD44+ tumor cells. CD133+CD44+ and CD133+CD44- tumor cells were isolated from three human metastatic hepatocellular carcinoma specimens. A 76-gene consensus signature was identified that distinguished between CD133+CD44+ and CD133+CD44- subgroups. CD133+CD44+ and CD133+CD44- subgroups from different patients were well clustered as two distinct classes according to this signature, and many genes in this signature were reported involved in tumor metastasis. Expression of four genes (CCL4, DKK3, CCR5 and MMP12) from this signature was confirmed in another three metastatic HCC specimens by real-time PCR. CD133+CD44+ and CD133+CD44- subpopulations of hepatocellular carcinoma were isolated from three metastatic hepatocellular carcinoma specimens by flow cytometry. A total of 30K to 50K cells for each subgroup was obtained for each microarray.
Project description:The purpose of this study is to screen for microRNAs related to lymphatic metastasis in mouse Hepatocellular Carcinoma cells, named H22, Hepa1-6, Hca-P, and Hca-F. The lymphatic metastasis abilities of the cell lines are different.
Project description:Six pairs of hepatocellular carcinoma and their corresponding non-tumrous liver parenchymas were analyzed to identify the genes differentially expressed in hepatocellular carcinoma and nontumorous liver parenchyma.
Project description:We report the different genes expression profile of mRNA in HCC cell lines. we constructed three kinds of cell lines, including control/USP39-KO/SIRT7-KO.
Project description:We sought to find out the molecular mechanism of CENPK displayed in hepatocellular carcinoma. Microarray experiments were carried out to identify different gene expression between CENPK-knockdown BEL-7404 cell line and Scramble BEL-7404 cell lines.
Project description:The incidence of TP53 loss-of-function in hepatocellular carcinoma is very high. In order to clarify the gene expression differences induced by the changes of TP53 gene, we used two human hepatocellular carcinoma cell lines, SK-HEP-1 and Hep 3B with TP53 knockdown or overexpression for RNA sequencing . SK-HEP-1 is a TP53 wild-type hepatocellular carcinoma cell line. Thus, we knockdown TP53 in SK-HEP-1. Hep 3B is a TP53 loss-of-function hepatocellular carcinoma cell line. Thus, we overexpress TP53 in Hep 3B. Results of RNA-seq analysis showed the differences after knocking-down or overexpressing TP53.
Project description:To demonstrate CD133+CD44+ and CD133+CD44- subpopulations of hepatocellular carcinoma as distinct subgroups, we have employed whole genome microarray expression profiling as a discovery platform to reveal the gene profiles of different subgroups and identify genes responsible for the enhanced metastatic potentials of CD133+CD44+ tumor cells. CD133+CD44+ and CD133+CD44- tumor cells were isolated from three human metastatic hepatocellular carcinoma specimens. A 76-gene consensus signature was identified that distinguished between CD133+CD44+ and CD133+CD44- subgroups. CD133+CD44+ and CD133+CD44- subgroups from different patients were well clustered as two distinct classes according to this signature, and many genes in this signature were reported involved in tumor metastasis. Expression of four genes (CCL4, DKK3, CCR5 and MMP12) from this signature was confirmed in another three metastatic HCC specimens by real-time PCR.
Project description:Six pairs of hepatocellular carcinoma and their corresponding non-tumrous liver parenchymas were analyzed to identify the genes differentially expressed in hepatocellular carcinoma and nontumorous liver parenchyma. We analyzed mRNA expression pattern of 6 primary hepatocellular carcinomas and their corresponding nontumourous liver parenchyma. The specimens were obtained from a tissue bank in our hospital. All the clinical informations were de-linked from the specimens.