在大肠炎相关癌症的小鼠模型中,IKKbeta将炎症与瘤发生联系在一起
Florian R Greten1, Lars Eckmann, Tim F Greten
1Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, La Jolla 92093, USA.
Cell
|August 6, 2004
概括
在肠道上皮细胞中禁用IKK/NF-kappaB通路可以减少与炎症相关的瘤发病率. 然而,向髓状细胞通过减少生长因子来减少瘤大小.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 炎症与癌症有关,NF-kappaB信号发挥着关键作用.
- 伊卡帕B激酶 (IKK) 复合体在对炎症刺激的反应中激活NF-kappaB.
研究的目的:
- 研究IKKbeta在与炎症相关的瘤发生中的作用.
- 确定IKKbeta无活化对瘤发育的细胞类型特异性影响.
主要方法:
- 利用大肠炎相关的癌症小鼠模型.
- 在肠道上皮细胞和骨髓细胞中分别存在遗传删除的IKKbeta.
- 评估了炎症,瘤发生率,瘤大小和亡.
主要成果:
- 在上皮细胞中IKKbeta的删除通过增加亡来减少瘤发生率,而不会改变炎症.
- 骨髓细胞中的IKKbeta缺失通过减少促炎性细胞因子而减少瘤大小,而不会影响亡.
- 该IKK/NF-kappaB通路不同调节瘤发病和生长.
结论:
- 在不同的细胞类型中,特定的IKKbeta无活化可以减轻由炎症驱动的瘤.
- 在将炎症与癌症联系起来,IKKbeta的作用涉及到亡调节和细胞因子信号传递.
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