Helicobacter pylori (H. pylori) infection might activate nuclear factor-κB (NF-κB), an oxidant-sensitive transcription regulator of inducible expression of inflammatory genes such as cyclooxygenase-2 (COX-2). We studied the role of NF-κB on expression of COX-2 in H. pylori-stimulated gastric cancer cell lines by using antioxidants, glutathione (GSH), and N-acetylcysteine (NAC) as well as an NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC). Gastric adenocarcinoma cell lines derived from Caucasian (AGS) cells and Korean (SNU-484) cells were used to study the role of NF-κB on COX-2 expression by H. pylori. They were treated with GSH, NAC, or PDTC in the presence of H. pylori. mRNA expression and protein level for COX-2 were determined by Northern blot and RT-PCR analysis as well as Western blot analysis. NF-κB activation was examined by electrophoretic mobility shift assay. As a result, H. pylori induced a time-dependent expression of mRNA and protein for COX-2 via activation of NF-κB, which was inhibited by GSH, NAC, and PDTC in the cells. In conclusion, oxidant-sensitive transcription factor NF-κB may play a novel role in expression of COX-2 by H. pylori stimulation in gastric cancer cells.
|Number of pages||9|
|Journal||Journal of Environmental Pathology, Toxicology and Oncology|
|Publication status||Published - 2002 Jun 29|
All Science Journal Classification (ASJC) codes
- Pathology and Forensic Medicine
- Health, Toxicology and Mutagenesis