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首页> 外文期刊>Cancer Cell >IL-6 and Stat3 are required for survival of intestinal epithelial cells and development of colitis-associated cancer.
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IL-6 and Stat3 are required for survival of intestinal epithelial cells and development of colitis-associated cancer.

机译：IL-6和Stat3是肠道上皮细胞存活和结肠炎相关癌症发展所必需的。

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Colitis-associated cancer (CAC) is the most serious complication of inflammatory bowel disease. Proinflammatory cytokines have been suggested to regulate preneoplastic growth during CAC tumorigenesis. Interleukin 6 (IL-6) is a multifunctional NF-kappaB-regulated cytokine that acts on epithelial and immune cells. Using genetic tools, we now demonstrate that IL-6 is a critical tumor promoter during early CAC tumorigenesis. In addition to enhancing proliferation of tumor-initiating cells, IL-6 produced by lamina propria myeloid cells protects normal and premalignant intestinal epithelial cells (IECs) from apoptosis. The proliferative and survival effects of IL-6 are largely mediated by the transcription factor Stat3, whose IEC-specific ablation has profound impact on CAC tumorigenesis. Thus, the NF-kappaB-IL-6-Stat3 cascade is an important regulator of the proliferation and survival of tumor-initiating IECs.
机译：结肠炎相关癌症（CAC）是炎症性肠病最严重的并发症。已建议促炎细胞因子在CAC肿瘤发生过程中调节肿瘤前的生长。白介素6（IL-6）是一种多功能的NF-κB调节细胞因子，作用于上皮细胞和免疫细胞。使用遗传工具，我们现在证明IL-6是早期CAC肿瘤发生过程中的关键肿瘤启动子。除了增强肿瘤引发细胞的增殖外，固有层髓样细胞产生的IL-6还可以保护正常和恶变前的肠上皮细胞（IEC）免受凋亡。 IL-6的增殖和存活作用在很大程度上由转录因子Stat3介导，后者的IEC特异性消融对CAC的肿瘤发生具有深远的影响。因此，NF-κB-IL-6-Stat3级联是启动肿瘤的IECs增殖和存活的重要调节剂。

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