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首页> 外文期刊>Genomics >Gene expression profiling of hepatitis B- and hepatitis C-related hepatocellular carcinoma using graphical Gaussian modeling
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Gene expression profiling of hepatitis B- and hepatitis C-related hepatocellular carcinoma using graphical Gaussian modeling

机译：使用图形高斯建模的乙型肝炎和丙型肝炎相关的肝细胞癌的基因表达谱

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Background & aims: Gene expression profiling of hepatocellular carcinoma (HCC) and background liver has been studied extensively; however, the relationship between the gene expression profiles of different lesions has not been assessed. Methods: We examined the expression profiles of 34 HCC specimens (17 hepatitis B virus [HBV]-related and 17 hepatitis C virus [HCV]-related) and 71 non-tumor liver specimens (36 chronic hepatitis B [CH-B] and 35 chronic hepatitis C [CH-C]) using an in-house cDNA microarray consisting of liver-predominant genes. Graphical Gaussian modeling (GGM) was applied to elucidate the interactions of gene clusters among the HCC and non-tumor lesions. Results: In CH-B-related HCC, the expression of vascular endothelial growth factor-family signaling and regulation of T cell differentiation, apoptosis, and survival, as well as development-related genes was up-regulated. In CH-C-related HCC, the expression of ectodermal development and cell proliferation, wnt receptor signaling, cell adhesion, and defense response genes was also up-regulated. Many of the metabolism-related genes were down-regulated in both CH-B- and CH-C-related HCC. GGM analysis of the HCC and non-tumor lesions revealed that DNA damage response genes were associated with AP1 signaling in non-tumor lesions, which mediates the expression of many genes in CH-B-related HCC. In contrast, signal transducer and activator of transcription 1 and phosphatase and tensin homolog were associated with early growth response protein 1 signaling in non-tumor lesions, which potentially promotes angiogenesis, fibrogenesis, and tumorigenesis in CH-C-related HCC. Conclusions: Gene expression profiling of HCC and non-tumor lesions revealed the predisposing changes of gene expression in HCC. This approach has potential for the early diagnosis and possible prevention of HCC.
机译：背景与目的：肝细胞癌（HCC）和背景肝的基因表达谱已被广泛研究。然而，尚未评估不同病变的基因表达谱之间的关系。方法：我们检查了34例HCC标本（17例乙型肝炎病毒[HBV]相关和17例丙型肝炎[HCV]相关性）和71例非肿瘤肝标本（36例慢性乙型肝炎[CH-B]和35种慢性丙型肝炎[CH-C]），其内部基因芯片由肝脏为主的基因组成。应用图形高斯建模（GGM）阐明了HCC和非肿瘤病变之间基因簇的相互作用。结果：在CH-B相关的HCC中，血管内皮生长因子家族信号的表达以及对T细胞分化，凋亡和存活的调控以及与发育相关的基因均被上调。在CH-C相关的HCC中，外胚层发育和细胞增殖，wnt受体信号转导，细胞粘附和防御反应基因的表达也被上调。在CH-B-和CH-C相关的HCC中，许多与代谢相关的基因均下调。对肝癌和非肿瘤性病变的GGM分析表明，DNA损伤反应基因与非肿瘤性病变中的AP1信号传导相关，它介导了CH-B相关性肝癌中许多基因的表达。相反，信号转导和转录激活因子1和磷酸酶和张力蛋白同源物与非肿瘤病变中的早期生长反应蛋白1信号传导相关，这可能促进CH-C相关HCC的血管生成，纤维生成和肿瘤发生。结论：HCC和非肿瘤病变的基因表达谱揭示了HCC基因表达的诱因变化。这种方法具有早期诊断和预防HCC的潜力。

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