NSAIDs肿瘤预防作用的非COX-2依赖性途径研究
基本信息
结项摘要
NSAIDs具有重要的临床肿瘤预防功能，可抑制肿瘤发生发展、侵入转移、血管生成并参与免疫逃避。最初认为其功能依赖于抑制COX-2活性，但现有证据表明NSAIDs可不依赖于COX-2发挥作用，机制复杂，对此尚无统一认识。我们在胃癌研究中发现，NSAIDs以COX-2非依赖方式上调15-LOX-1、Bcl-2家族分子和caspases等的表达从而激活细胞凋亡和生长抑制。为澄清NSAIDs的作用机制，尤其是COX-2非依赖途径，为研发药物提供新的靶点，我们拟通过microarray和蛋白组分析方法，检测NSAIDs和COX-2基因阻断引发的胃癌细胞内基因转录和翻译改变；分析和归类所获得高通量信息；进一步验证关键的信号通路及相互间联系，从而全面揭示NSAIDs的信号网络，解释COX-2依赖性/非依赖性通路的选择，提供作为药物研发潜在新靶点的候选分子。
项目摘要
项目成果
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数据更新时间：2023-05-31
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