Department of Cellular and Moleculart Medicine, The University of Arizona, Tucson, AZ 85724, USA.
World J Gastroenterol. 2013 Apr 21;19(15):2307-12. doi: 10.3748/wjg.v19.i15.2307.
Barrett's esophagus (BE) is a metaplastic lesion of the distal esophagus arising as a consequence of chronic gastroesophageal reflux disease. Multiple studies show that BE is associated with increased risk of esophageal adenocarcinoma (EAC). Epidemiological studies and animal models demonstrate that chronic inflammation triggered by repeated exposure to refluxate predisposes to the development of BE and EAC. The chronic inflammation is associated with cytokine alterations. Interleukin 6 (IL-6) is a cytokine that stimulates cell proliferation and apoptosis resistance is frequently increased in different cancers. Importantly, IL-6 and transcriptional factor signal transducer and activator of transcription 3 (STAT3) that is activated by IL-6 are also increased in BE and EAC. This review critically appraises the role of IL-6/STAT3 pathway in progression of BE to EAC from the published evidence currently available.
巴雷特食管（BE）是一种远端食管的化生性病变，是由慢性胃食管反流病引起的。多项研究表明，BE 与食管腺癌（EAC）的风险增加有关。流行病学研究和动物模型表明，反复接触反流物引起的慢性炎症易导致 BE 和 EAC 的发生。这种慢性炎症与细胞因子的改变有关。白细胞介素 6（IL-6）是一种细胞因子，可刺激细胞增殖，细胞凋亡抵抗在不同的癌症中经常增加。重要的是，IL-6 和转录因子信号转导和转录激活因子 3（STAT3）也在 BE 和 EAC 中增加，IL-6 可激活 STAT3。本综述从现有文献中批判性地评价了 IL-6/STAT3 通路在 BE 进展为 EAC 中的作用。
