Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, China.
Mediators Inflamm. 2017;2017:5126048. doi: 10.1155/2017/5126048. Epub 2017 Aug 9.
Patients with inflammatory bowel disease (IBD) are at an increased risk of developing colorectal cancer (CRC). The risk factors of CRC in IBD patients include long disease duration, extensive colitis, severe histological inflammation, and coexistence with primary sclerosing cholangitis (PSC). Several molecular pathways that contribute to sporadic CRC are also involved in the pathogenesis of colitis-associated CRC. It is well established that long-standing chronic inflammation is a key predisposing factor of CRC in IBD. Proinflammatory pathways, including nuclear factor kappa B (NF-B), IL-6/STAT3, cyclooxygenase-2 (COX-2)/PGE, and IL-23/Th17, promote tumorigenesis by inducing the production of inflammatory mediators, upregulating the expression of antiapoptotic genes, and stimulating cell proliferation as well as angiogenesis. Better understanding of the underlying mechanisms may provide some promising targets for prevention and therapy. This review aims to elucidate the role of these signaling pathways in the pathogenesis of colitis-associated CRC using evidence-based approaches.
炎症性肠病（IBD）患者发生结直肠癌（CRC）的风险增加。IBD 患者发生 CRC 的危险因素包括疾病病程长、广泛性结肠炎、严重的组织学炎症以及合并原发性硬化性胆管炎（PSC）。导致散发性 CRC 的几个分子途径也参与了结肠炎相关性 CRC 的发病机制。长期慢性炎症是 IBD 中 CRC 的一个关键诱发因素，这一点已得到充分证实。促炎途径，包括核因子 kappa B（NF-κB）、IL-6/STAT3、环氧化酶-2（COX-2）/PGE2 和 IL-23/Th17，通过诱导炎症介质的产生、上调抗凋亡基因的表达以及刺激细胞增殖和血管生成来促进肿瘤发生。更好地了解潜在机制可能为预防和治疗提供一些有希望的靶点。本综述旨在使用循证方法阐明这些信号通路在结肠炎相关性 CRC 发病机制中的作用。
