作者: Byron Cryer , Stuart Jon Spechler , Kenneth Shewmake , Rhonda F. Souza , David G. Beer
DOI:
关键词: Cell growth 、 Biology 、 Carcinogenesis 、 Epithelium 、 Cancer research 、 Endocrinology 、 Cell culture 、 Programmed cell death 、 Esophageal disease 、 Internal medicine 、 Apoptosis 、 Adenocarcinoma
摘要: Adenocarcinoma in Barrett's esophagus has been increasing incidence at a rapid rate for more than two decades. Cyclooxygenase (COX)-2 appears to play an important role gastrointestinal carcinogenesis, and COX-2 overexpression demonstrated both esophageal adenocarcinomas the metaplastic epithelium of esophagus. The aim our study was determine whether selective inhibition by NS-398 would alter rates cell growth apoptosis human Barrett's-associated adenocarcinoma lines. COX-1 expression lines determined using reverse transcription-PCR Western blotting mRNA protein, respectively. Esophageal were treated with various concentrations (selective inhibition) flurbiprofen inhibition). Cell compared flurbiprofen-treated untreated tumor lines; NS-398-treated protein detected three (SEG-1 FLO); third line, BIC-1, did not express or under basal conditions after stimulation phorbol 12-myristate 13-acetate. Treatment COX-1-selective affect any In contrast, treatment COX-2-selective significantly suppressed increased that expressed FLO), but line (BIC-1). We conclude administration inhibitor decreases increases cells COX-2. These observations suggest potential inhibitors prevention patients