Jian Cheng, Xiao-Ming Fan, Department of Gastroenterology and Hepatology, Jinshan Hospital of Fudan University, Shanghai 201508, China.
World J Gastroenterol. 2013 Nov 14;19(42):7361-8. doi: 10.3748/wjg.v19.i42.7361.
Although the incidence of gastric cancer has been declining in recent decades, it remains a major public health issue as the second leading cause of cancer death worldwide. In China, gastric cancer is still the main cause of death in patients with malignant tumors. Most patients are diagnosed at an advanced stage and mortality is high. Cyclooxygenase-2 (COX-2) is a rate-limiting enzyme in prostanoid synthesis and plays an important role in the development and progression of gastric cancer. The expression of COX-2 in gastric cancer is upregulated and its molecular mechanisms have been investigated. Helicobacter pylori infection, tumor suppressor gene mutation and the activation of nuclear factor-kappa B may be responsible for the elevated expression of COX-2 in gastric cancer. The mechanisms of COX-2 in the development and progression of gastric cancer are probably through promoting the proliferation of gastric cancer cells, while inhibiting apoptosis, assisting angiogenesis and lymphatic metastasis, and participating in cancer invasion and immunosuppression. This review is intended to discuss, comment and summarize recent research progress on the role of COX-2 in gastric cancer development and progression, and elucidate the molecular mechanisms which might be involved in the carcinogenesis.
尽管近年来胃癌的发病率有所下降，但它仍是一个主要的公共卫生问题，是全球癌症死亡的第二大主要原因。在中国，胃癌仍然是恶性肿瘤患者死亡的主要原因。大多数患者在晚期被诊断出来，死亡率很高。环氧化酶-2（COX-2）是前列腺素合成的限速酶，在胃癌的发生和发展中起着重要作用。COX-2 在胃癌中的表达上调，其分子机制已被研究。幽门螺杆菌感染、肿瘤抑制基因突变和核因子-κB 的激活可能导致胃癌中 COX-2 的表达升高。COX-2 在胃癌发生和发展中的作用机制可能是通过促进胃癌细胞的增殖，同时抑制细胞凋亡，辅助血管生成和淋巴转移，并参与癌症侵袭和免疫抑制。本文旨在讨论、评价和总结 COX-2 在胃癌发生和发展中的作用的最新研究进展，并阐明可能涉及致癌作用的分子机制。
