摘要
近年来,由于工业发展负面影响造成的环境污染及吸烟等不良嗜好导致吸入人体肺部的致癌物急剧增加,致使肺癌的发病率及死亡率逐年升高,已跃居各癌症之首.研究表明,环境致癌物诱导肺部慢性炎症与肺癌的发生发展之间存在着紧密联系,环境致癌物如砷、镍及苯并芘等暴露可激活NFAT、NF-κB、AP-1等转录因子,调控炎症因子如TNFα及COX-2等的表达,且这些炎性因子的释放又可正反馈激活转录因子,促进更多的炎性因子产生,进而形成炎性因子产生回路,维持肺部炎性微环境,从而促进肺癌的发生发展.本文就环境致癌物诱导肺部炎症导致肺癌发生发展的分子机制及其相关信号通路进行了综述.
Air pollution from rapid industrialization in China and cigarette smoking led to increased environmental exposure to carcinogens, such as Benzo（a）pyrene （B [a]P）, nickel, arsenic, can increase the risk for lung cancer. And lung cancer has replaced liver cancer as the leading cause of death among the patients with malignant tumors in China. According to recent studies, carcinogens play major roles in the development of lung cancer and chronic inflammation mediates the carcinogenesis partly. Carcinogen exposure could activate the transcription factor such as NFAT, NF-KB, AP-1 that will enhance inflammation factor transcription and then increase their release. Moreover, this process will be promoted by creating a positive regulatory loop due to sustained activation of transcription factor from the stimulation of inflammation factor release. The chronically inflammational microenvironment induced by carcinogen will cause the initiation and development of lung cancer. The review summarizes the cellular and animal evidences linking chronic inflammation induced by environmental carcinogens to lung cancer.
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
2014年第1期41-51,共11页
Progress In Biochemistry and Biophysics
基金
国家自然科学基金(9102970
81229002)资助项目~~
关键词
环境致癌物
炎症
恶性转化
肺癌
carcinogens, inflammation, transformation, lung cancer
