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作 者:曹薇[1] 张道荣[1] 乔菊久[1] 方长青[1] 侯锐[2]
机构地区:[1]中国医科大学基础医学院病理教研室,沈阳110001 [2]中国医科大学附属第二医院胸外科
出 处:《中国肺癌杂志》2006年第5期418-422,共5页Chinese Journal of Lung Cancer
摘 要:背景与目的Pin1是人类的肽基脯氨酰异构酶,它使磷酸化的丝氨酸/苏氨酸—脯氨酰键异构化,调节磷酸化蛋白质活性,对人类恶性肿瘤的发生发展具有重要作用。本研究的目的是探讨Pin1在肺鳞癌和肺腺癌组织中的表达及其与肺癌临床病理学特征的关系,并分析其与β-连环素(β-catenin)是否存在相关性。方法应用免疫组织化学(SP法)和Westernblot法,检测肺癌组织和正常肺组织中Pin1和β-catenin表达情况,并结合临床和病理资料进行分析。结果免疫组化结果显示:Pin1在78.3%(54/69)的肺癌组织中过度表达,β-catenin在63.8%(44/69)的肺癌组织中异常蓄积。Pin1和β-catenin表达水平与患者的性别、年龄、肺癌组织学分型、有无淋巴结转移和TNM分期等临床病理学特征无明显关系。Pin1的过度表达与β-catenin异常蓄积呈正相关(P<0.05)。Westernblot结果显示:Pin1和β-catenin在肺癌组织中的表达水平均高于正常肺组织(P<0.05)。结论在肺鳞癌和肺腺癌中,Pin1的过度表达可能直接导致肺癌的发生。Pin1对β-catenin的影响可能是Pin1发挥作用的机制之一。Background and objective The conformation of a subset of phosphorylated serines or threo nines preceding proline motifs is regulated by the prolyl isomerase Pinl. Pinl playsa critical role in oncogenesis. The aim of this study is to explore the relationship between the expression of Pinl and clinicopathological factors in squamous cell carcinoma and adenocarcinoma of the lung, and to analyze the correlation between Pinl and β-catenin. Methods The expression of Pinl and β-catenin proteins was detected in 69 lung cancer cases by immunohistochemical SP method, and in 30 fresh lung samples by Western blot. Results Immunohistochemically, the ovcrcxpression of Pinl and β-catenin in lung cancer was 78.3% (54/69) and 63.8% (44/69). respectively. The expression of Pinl and β- catenin was not related to age, sex, histological classification, differ entiation, lymph node metastasis and pTNM stages. There was a positive correlation between overexpression of Pinl and aberrant β-catenin expression (P〈0.05). Western blot results showed that the expression of Pinl and β-catenin in lung cancer tissues was significantly higher than that of paracancerous lung tissues (P〈 0.05). Conclusion Pinl is overexpressed in squamous cell carcinoma and adenocarcinoma of the lung and may play a critical role in oncogenesis of lung cancer. Overexpression of Pinl might contribute to the upregulation of β-eatenin and it may be one of the pathways for Pinl to work.
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