Gene Expression Profile Related to the Progression of Preneoplastic Nodules toward Hepatocellular Carcinoma in Rats
Autor: | Julio Isael Pérez-Carréon, Cristina López-García, Samia Fattel-Fazenda, Evelia Arce-Popoca, Leticia Alemán-Lazarini, Sergio Hernández-García, Véronique Le Berre, Sergueï Sokol, Jean Marie Francois, Saúl Villa-Treviño |
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Jazyk: | angličtina |
Rok vydání: | 2006 |
Předmět: | |
Zdroj: | Neoplasia: An International Journal for Oncology Research, Vol 8, Iss 5, Pp 373-383 (2006) |
Druh dokumentu: | article |
ISSN: | 1476-5586 1522-8002 |
DOI: | 10.1593/neo.05841 |
Popis: | In this study, we investigated the time course gene expression profile of preneoplastic nodules and hepatocellular carcinomas (HCC) to define the genes implicated in cancer progression in a resistant hepatocyte model. Tissues that included early nodules (1 month, ENT-1), persistent nodules (5 months, ENT-5), dissected HCC (12 months), and normal livers (NIL) from adult rats were analyzed by cDNA arrays including 1185 rat genes. Differential genes were derived in each type of sample (n = 3) by statistical analysis. The relationship between samples was described in a Venn diagram for 290 genes. From these, 72 genes were shared between tissues with nodules and HCC. In addition, 35 genes with statistical significance only in HCC and with extreme ratios were identified. Differential expression of 11 genes was confirmed by comparative reverse transcription-polymerase chain reaction, whereas that of 2 genes was confirmed by immunohistochemistry. Members involved in cytochrome P450 and second-phase metabolism were downregulated, whereas genes involved in glutathione metabolism were upregulated, implicating a possible role of glutathione and oxidative regulation. We provide a gene expression profile related to the progression of nodules into HCC, which contributes to the understanding of liver cancer development and offers the prospect for chemoprevention strategies or early treatment of HCC. |
Databáze: | Directory of Open Access Journals |
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