Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiling of HCC vs. Normal liver and Pericancer vs. Normal liver.

ABSTRACT: Hepatocellular carcinoma (HCC) is one of the most malignant and lethal cancers in the world. Its complex process of molecular pathogenesis indicates that HCC is caused by multiple etiological factors and involves multiple types of genes during its development and progression. In the current study, we performed a microarray analysis on the mRNA transcriptome of HCC (C), peri-cancerous liver (P) and normal liver (N) tissues. After integrating these results with information from the Gene Ontology and KEGG Pathway databases, we analyzed the potential interactions between different genes and constructed an interaction network, and identified the regulator, mediator and effector genes in this interaction network. Three types of tissues: 49 pairs of homogenous human primary hepatocellular carcinoma (Cancer, C) and pericancer liver tissues (Pericancer, P), 10 normal liver tissues (Normal, N). Three-condition experiment, HCC vs. Normal and Pericancer vs. Normal.

ORGANISM(S): Homo sapiens

SUBMITTER: Lin Wei

PROVIDER: E-GEOD-45114 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Purpose: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-associated mortality worldwide. Although the molecular mechanisms underpinning HCC are unknown, gene copy number and associated mRNA expression changes are frequently reported. Experimental Design: Comparative genomic hybridization arrays spotted with 4,041 bacterial artificial chromosome clones were used to assess copy number changes in 45 HCC tissues to identify chromosomal regions associated with the pathogenesis of HCC. Seventy more HCC tissues were used to validate candidate genes by using western blots and immunohistochemistry. Results: A total of 259 clones were associated with copy number changes that significantly differed between normal liver and HCC samples. The chromosomal region 1q32.1 containing the nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) gene was associated with tumor vascular invasion. Western blot analysis demonstrated that NUCKS1 was up-regulated in 37 of 70 (52.8%) HCC tissues compared with adjacent non-tumor tissues, and over-expressed in a vast majority of HCCs (44/52, 84.6%) as determined by immunohistochemical staining. Furthermore, immunostaining of both NUCKS1 and glypican-3 improved the diagnostic prediction of HCC. Knock-down of NUCKS1 by siRNA decreased the cell viability of the Hep3B cell line and reduced tumor formation in a xenograft mouse model. Functional enrichment analysis revealed the association of NUCKS1 with signal transduction, immunity and defense, and nucleotide metabolism pathways. Conclusions: NUCKS1 was identified as a potential oncogene at chromosomal 1q32.1 in patients with HCC, and it might be a valuable immunodiagnostic marker for HCC. Comparative genomic hybridization arrays spotted with 4,041 bacterial artificial chromosome clones were used to assess copy number changes in 45 HCC tissues and 25 normal liver tissues to identify chromosomal regions associated with the pathogenesis of HCC

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Transcriptional profiling of HCC vs. Normal liver and Pericancer vs. Normal liver.

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