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Expression profiles of hepatocellular carcinomas derived from ductular progenitor cells

ABSTRACT: Hepatocellular carcinoma (HCC) generally arises in chronically inflamed liver and is thought to originate from regenerating liver cells that acquired genetic alterations. Both hepatocytes and ductular progenitor cells (DPCs) contribute to liver regeneration and are candidate cellular origins of HCCs. In the current study, we used lineage-tracing analysis to show that Epcam-expressing DPCs give rise to HCCs in inflamed liver. Under conditions in which proliferating DPCs differentiate into cholangiocytes but not into hepatocytes, the accumulation of genetic alterations in Epcam-expressing DPCs resulted in the development of HCCs with histologic features of concomitant ductule-like structures resembling human cholangiolocellular carcinoma (CLC). To elucidate the characteristics of DPC-derived HCC, gene expression of HCCs derived from Epcam-expressing DPCs were evaluated using Agilent SurePrint G3 Mouse Gene Expression 8x60K v2. Two DPC-derived HCCs with CLC components, two DPC-derived HCCs without CLC, and two HCCs derived from albumin-expressing cells were analyzed.

ORGANISM(S): Mus musculus

PROVIDER: GSE95099 | GEO | 2020/02/19

REPOSITORIES: GEO

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Project description:Chronic infections by hepatitis B virus (HBV) and hepatitis C virus (HCV) appear to be the most significant causes of hepatocellular carcinoma (HCC). Aberrant promoter methylation is known to be deeply involved in cancer, including HCC. In this study, we analyzed aberrant promoter methylation on genome-wide scale in 6 HCCs including 3 HBV-related and 3 HCV-related HCCs, 6 matched noncancerous liver tissues and 3 normal liver tissues by methylated DNA immunoprecipitation-on-chip analysis. Candidate genes with promoter methylation were detected more frequently in HCV-related HCC. Candidate genes methylated preferentially to HBV-related or HCV-related HCCs were detected and selected, and methylation levels of the selected genes were validated using 125 liver tissue samples, including 61 HCCs (28 HBV-related HCCs and 33 HCV-related HCCs) and matched 59 matched noncancerous livers, and 5 normal livers, by quantitative methylation analysis using MALDI-TOF mass spectrometry. Among analyzed genes, preferential methylation in HBV-related HCC was validated in 1 gene only. However, 15 genes were found methylated preferentially in HCV-related HCC, which was independent from age. Hierarchical clustering of HCC using these 15 genes stratified HCV-related HCC as a cluster of frequently methylated samples. The 15 genes included genes inhibitory to cancer-related signaling such as RAS/RAF/ERK and Wnt/b-catenin pathways. It was indicated that genes methylated preferentially in HCV-related HCC exist, and it was suggested that DNA methylation might play an important role in HCV-related HCC by silencing cancer-related pathway inhibitors. we analyzed aberrant promoter methylation in 6 HCC clinical samples (including 3 HBV-related HCCs and 3 HCV-related HCCs) and their matched noncancerous tissues on genome-wide scale by the method. Candidate regions of promoter methylation preferentially to HBV-related HCC and HCV-related HCC were selected, and the methylation levels of these genes were measured quantitatively using MALDI-TOF mass spectrometry. Expression levels of these 6 pairs of HCC and 4 more pairs of HCCs and surrounding noncancerous tissues were analyzed by expression array and are reported in this Series. <br><br>This experiment was reloaded in November 2010 after additional curation. this dataset is part of the TransQST collection.

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Expression profiles of hepatocellular carcinomas derived from ductular progenitor cells

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