Department of General Surgery, Shengjing Hospital, China Medical University, Shenyang, Liaoning Province, China.
Department of Gastrointestinal Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Inflamm Bowel Dis. 2019 Sep 18;25(10):1595-1602. doi: 10.1093/ibd/izz149.
Dysregulated inflammatory responses play a pivotal role in the initiation, development, and progression of tumors, as demonstrated by the association between ulcerative colitis and the increased risk of colon carcinoma. In this review, the underlying mechanisms for the initiation and development of ulcerative colitis and colitis-associated cancer are described, mainly focusing on the inflammation and inflammatory cytokine. Disruption of the intestinal mucosal barrier and bacterial invasion resulted in intestinal inflammation; and further TLR4/NF-κB stimulation in intestinal epithelial cells, inflammatory cell infiltration, and inflammatory cytokine release all confer survival advantages to or promote abnormal proliferation in susceptible cells. Importantly, the respective roles of TLR4/NF-κB, TNF-α, and IL-6 in intestinal epithelial cells and inflammatory cells are summarized in detail. A thorough understanding of these molecular mechanisms may help researchers and clinicians to explore novel approaches for the prevention and treatment of colitis-associated cancer.
失调的炎症反应在肿瘤的发生、发展和进展中起着关键作用，溃疡性结肠炎与结肠癌风险增加之间的关联就证明了这一点。在这篇综述中，描述了溃疡性结肠炎和结肠炎相关癌症发生和发展的潜在机制，主要集中在炎症和炎症细胞因子上。肠道黏膜屏障的破坏和细菌入侵导致肠道炎症；而 TLR4/NF-κB 在肠道上皮细胞中的进一步刺激、炎症细胞浸润和炎症细胞因子释放都为易感细胞的存活优势或异常增殖提供了帮助。重要的是，详细总结了 TLR4/NF-κB、TNF-α 和 IL-6 在肠道上皮细胞和炎症细胞中的各自作用。深入了解这些分子机制可能有助于研究人员和临床医生探索预防和治疗结肠炎相关癌症的新方法。
