...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Inflammation-induced tumorigenesis in the colon is regulated by caspase-1 and NLRC4
【24h】

Inflammation-induced tumorigenesis in the colon is regulated by caspase-1 and NLRC4

机译：结肠中炎症诱导的肿瘤发生受caspase-1和NLRC4调控

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Chronic inflammation is a known risk factor for tumorigenesis, yet the precise mechanism of this association is currently unknown. The inflammasome, a multiprotein complex formed by NOD-like receptor (NLR) famify members, has recently been shown to orchestrate multiple innate and adaptive immune responses, yet its potential role in inflammation-induced cancer has been little studied. Using the azoxymethane and dextran sodium sulfate colitis-associated co-lorectal cancer model, we show that caspase-1-deficient (Casp1~(-/-)) mice have enhanced tumor formation. Surprisingly, the role of caspase-1 in tumorigenesis was not through regulation of colonic inflammation, but rather through regulation of colonic epithelial cell proliferation and apoptosis. Consequently, caspase-1-deficient mice demonstrate increased colonic epithelial cell proliferation in early stages of injury-induced tumor formation and reduced apoptosis in advanced tumors. We suggest a model in which the NLRC4 inflammasome is central to colonic inflammation-induced tumor formation through regulation of epithelial cell response to injury.
机译：慢性炎症是已知的肿瘤发生危险因素，但是这种关联的确切机制目前尚不清楚。炎症小体是由NOD样受体（NLR）形成成员的多蛋白复合物组成，最近已显示出能协调多种先天性和适应性免疫应答，但对其在炎症诱导的癌症中的潜在作用尚未进行研究。使用乙氧基甲烷和右旋糖酐硫酸钠结肠炎相关的结肠直肠癌模型，我们表明缺乏caspase-1缺陷的小鼠（Casp1〜（-/-））具有增强的肿瘤形成。令人惊讶地，caspase-1在肿瘤发生中的作用不是通过调节结肠炎症，而是通过调节结肠上皮细胞增殖和凋亡。因此，caspase-1缺陷小鼠在损伤诱导的肿瘤形成早期显示出结肠上皮细胞增殖增加，而晚期肿瘤的凋亡减少。我们提出了一个模型，其中NLRC4炎性小体通过调节上皮细胞对损伤的反应，对结肠炎症诱导的肿瘤形成至关重要。

著录项

  • 来源
  • 作者

    Bo Hu; Eran Elinav; Samuel Huber; Carmen J. Booth; Till Strowig; Chengcheng Jin; Stephanie C. Eisenbarth; Richard A. Flavell;

  • 作者单位

    Department of Immunobiology,Yale University School of Medicine, New Haven, CT 06520,Department of Molecular Biophysics and Biochemistry,Yale University School of Medicine, New Haven, CT 06520;

    Department of Immunobiology,Yale University School of Medicine, New Haven, CT 06520;

    Department of Immunobiology,Yale University School of Medicine, New Haven, CT 06520;

    Section of Comparative Medicine,Yale University School of Medicine, New Haven, CT 06520;

    Department of Immunobiology,Yale University School of Medicine, New Haven, CT 06520;

    Department of Immunobiology,Yale University School of Medicine, New Haven, CT 06520,Department of Molecular Biophysics and Biochemistry,Yale University School of Medicine, New Haven, CT 06520;

    Department of Immunobiology,Yale University School of Medicine, New Haven, CT 06520,Department of Laboratory Medicine,Yale University School of Medicine, New Haven, CT 06520;

    Department of Immunobiology,Yale University School of Medicine, New Haven, CT 06520,Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    colon cancer; inflammation-induced colorectal cancer; NLR family; pyrin domain containing 3;

    机译：结肠癌;炎症性大肠癌;NLR家族;含3个吡啶域;

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号