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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >A role of histone H4 hypoacetylation in vascular endothelial growth factor expression in colon mucosa adjacent to implanted cancer in athymic mice cecum.
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A role of histone H4 hypoacetylation in vascular endothelial growth factor expression in colon mucosa adjacent to implanted cancer in athymic mice cecum.

机译：组蛋白H4乙酰化过低在无胸腺小鼠盲肠移植癌附近结肠黏膜血管内皮生长因子表达中的作用。

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Expression of angiogenic factors is upregulated in hyperplastic mucosa adjacent to colon cancer, and this upregulation is closely associated with cancer growth and metastasis. We investigated the role of histone acetylation in vascular endothelial growth factor (VEGF) expression in hyperplastic mucosa adjacent to orthotopic colon cancer in mice. In the hyperplastic mucosa adjacent to KM12SM tumor in the cecum of athymic mice, VEGF upregulation was associated with hypoxia-inducible factor (HIF)-1alpha induction. The hyperplastic mucosa also showed hypoacetylation of histone H4 and reduction of both p53 and von Hippel-Lindau (VHL) proteins. To examine the effects of growth factors and cytokines on histone acetylation and levels of p53, VHL and HIF-1alpha, the rat intestinal epithelial cell line IEC6 was treated with epidermal growth factor (EGF) and interleukin (IL)-15 for 35 days. Acetylated histone H4, p53 protein and ubiquitinated protein levels were reduced, whereas HIF-1alpha production was upregulated in EGF- and IL-15-treated IEC6 cells. These findings suggest that EGF- or IL-15-induced histone H4 hypoacetylation is associated with repression of p53 and VHL genes in intestinal epithelial cells. The subsequent suppression of protein ubiquitination leads to upregulation of VEGF production by HIF-1alpha retention.
机译：在邻近结肠癌的增生性粘膜中，血管生成因子的表达上调，并且这种上调与癌症的生长和转移密切相关。我们调查了组蛋白乙酰化在邻近小鼠原位结肠癌的增生性粘膜中血管内皮生长因子（VEGF）表达中的作用。在无胸腺小鼠盲肠的KM12SM肿瘤附近的增生性黏膜中，VEGF的上调与缺氧诱导因子（HIF）-1α的诱导有关。增生性粘膜还显示出组蛋白H4的乙酰化过低，p53和von Hippel-Lindau（VHL）蛋白均降低。为了检查生长因子和细胞因子对组蛋白乙酰化和p53，VHL和HIF-1alpha水平的影响，将大鼠肠上皮细胞系IEC6分别用表皮生长因子（EGF）和白介素（IL）-15处理35天。乙酰化的组蛋白H4，p53蛋白和泛素化蛋白水平降低，而HIF-1alpha产生在经EGF和IL-15处理的IEC6细胞中上调。这些发现表明，EGF或IL-15诱导的组蛋白H4过乙酰化与肠上皮细胞中p53和VHL基因的抑制有关。随后的蛋白泛素化抑制导致HIF-1alpha保留导致VEGF产生上调。

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