Open AccessRole of interleukin-6 in Barrett’s esophagus pathogenesis
Author(s) -
Katerina Dvorak,
Bohuslav Dvořák
Publication year - 2013
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v19.i15.2307
Subject(s) - stat3 , esophagus , medicine , cytokine , inflammation , stat protein , pathogenesis , barrett's esophagus , interleukin 6 , interleukin 9 , interleukin , interleukin 23 , adenocarcinoma , cancer research , apoptosis , immunology , gastroenterology , pathology , cancer , biology , biochemistry
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.