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首页> 外文期刊>World Journal of Gastroenterology >Tumor metastasis and the reciprocal regulation of heparanase gene expression by nuclear factor kappa B in human gastric carcinoma tissue.
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Tumor metastasis and the reciprocal regulation of heparanase gene expression by nuclear factor kappa B in human gastric carcinoma tissue.

机译：核转移因子κB在人胃癌组织中的肿瘤转移和乙酰肝素酶基因表达的相互调节。

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AIM: To investigate whether NF-kappaB is activated in human gastric carcinoma tissues and, if so, to study whether there is any correlation between NF-kappaB activity and heparanase expression in gastric carcinoma. METHODS: NF-kappaB activation was assayed by immunohistochemical staining in formalin-fixed, paraffin-embedded specimens from 45 gastric carcinoma patients. Electrophoretic mobility shift assay (EMSA) method was used for nuclear protein from these fresh tissue specimens. Heparanase gene expression was quantified using quantitative RT-PCR. RESULTS: The nuclear translocation of RelA (marker of NF-kappaB activation) was significantly higher in tumor cells compared to adjacent and normal epithelial cells ((41.3+/-3.52)% vs (0.38+/-0.22) %, t = 10.993, P = 0.000<0.05; (41.3+/-3.52)% vs (0+/-0.31)%, t = 11.484, P = 0.000<0.05). NF-kappaB activation was correlated with tumor invasion-related clinicopathological features such as lymphatic invasion, pathological stage, and depth of invasion (Z = 2.148, P = 0.032<0.05; chi(2) = 8.758, P = 0.033<0.05; chi(2) = 18.531, P = 0.006<0.05). NF-kappaB activation was significantly correlated with expression of heparanase gene (r = 0.194, P = 0.046<0.05). CONCLUSION: NF-kappaB RelA (p65) activation was related with increased heparanase gene expression and correlated with poor clinicopathological characteristics in gastric cancers. This suggests NF-kappaB as a major controller of the metastatic phenotype through its reciprocal regulation of some metastasis-related genes.
机译：目的：研究人胃癌组织中NF-κB是否被激活，如果是，则研究胃癌中NF-κB活性与乙酰肝素酶表达之间是否存在相关性。方法：采用免疫组织化学染色法对45例胃癌患者的福尔马林固定，石蜡包埋的标本进行了NF-κB活化分析。电泳迁移率移动分析（EMSA）方法用于从这些新鲜组织标本中提取核蛋白。使用定量RT-PCR对乙酰肝素酶基因表达进行定量。结果：与邻近和正常上皮细胞相比，肿瘤细胞中RelA（NF-κB激活的标志物）的核易位明显更高（（41.3 +/- 3.52）％vs（0.38 +/- 0.22）％，t = 10.993 ，P ＝ 0.000 ＜0.05；（41.3 +/- 3.52）％对（0 +/- 0.31）％，t ＝ 11.484，P ＝ 0.000 ＜0.05）。 NF-κB活化与肿瘤浸润相关的临床病理特征如淋巴管浸润，病理分期和浸润深度有关（Z = 2.148，P = 0.032 <0.05; chi（2）= 8.758，P = 0.033 <0.05; chi （2）= 18.531，P = 0.006 <0.05）。 NF-κB活化与乙酰肝素酶基因表达显着相关（r = 0.194，P = 0.046 <0.05）。结论：NF-κBRelA（p65）激活与胃癌中乙酰肝素酶基因表达增加有关，并且与不良的临床病理特征有关。这表明NF-kappaB通过相互调节某些与转移相关的基因而成为转移表型的主要控制者。

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