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当代肿瘤药物靶点

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ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

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Research Article

TOM34，AL1A1，PADI2和KLRBA在NNK诱导的Wistar大鼠肺癌中的差异表达及其意义

卷 19, 期 11, 2019

页: [919 - 929] 页: 11

弟呕挨: 10.2174/1871525717666190717162646

价格: $65

摘要

背景：肺癌是死亡率最高的最常见癌症。仅在晚期进行诊断和缺乏有效治疗是导致高死亡率的主要因素。烟草烟雾是导致肺部炎症和肿瘤发展的主要因素。 目的：进行本研究以鉴定差异表达的蛋白质，并阐明其在癌变过程中的作用。 方法：以NNK为致癌物在Wistar大鼠中发展肺癌，并通过组织病理学检查证实其发展。二维SDS PAGE用于分析总蛋白并找出NNK处理的肺组织相对于对照组织的差异表达蛋白。蛋白质组学分析的结果通过使用实时荧光定量PCR定量相应的转录本进一步得到验证。最后，使用Cytoscape查找蛋白质与蛋白质的相互作用。 结果：NNK治疗后第9个月的组织病理学检查显示有肿瘤。蛋白质组学分析显示了几种差异表达的蛋白质，其中四个被选作进一步研究。在NNK处理的肺组织中上调的TOM34，AL1A1，PADI2和KLRBA实时分析显示编码所选蛋白质的基因过表达。因此，蛋白质组和转录组数据相互证实。此外，这些蛋白显示出与NF-κB家族成员和STAT3的相互作用。 结论：我们得出结论，这些蛋白在通过NF-κB和STAT3途径诱导肺癌中起重要作用。因此，这些可能具有用作治疗靶点和早期检测肺癌的潜力。

关键词: 肺癌，TOM34，AL1A1，PADI2，KLRBA，蛋白质组学。

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