Wu C-S et al. (2007) Predictive role of nuclear factor-κB activity in gastric cancer: a promising adjuvant approach with caffeic acid phenethyl ester. J Clin Gastroenterol 41: 894–900

NF-κB expression correlates with tumor progression in several different cancers, but its role in gastric carcinoma is not clear. Now, a recent report from Wu et al. confirms that Helicobacter pylori induced NF-κB activation is related to chronic inflammation and carcinogenesis in gastric cancer.

Analysis of gastric tissue samples found that nuclear NF-κB expression was more common in cancer samples than in non-malignant samples (P = 0.0001). H. pylori infection is a well-known risk factor for gastric carcinoma and, in this study, 81% of the infected cancer specimens were also positive for NF-κB. To confirm this observation, the authors infected human gastric carcinoma cells with H. pylori in vitro and, as expected, observed an increase in NF-κB activation. This was associated with increased expression of the inflammatory cytokines IL-1 and IL-8, and the pro-metastatic enzyme matrix metalloprotease (MMP)-9. Returning to the tissue samples, reverse transcription polymerase chain reaction analysis revealed an elevated expression of these factors in gastric cancer compared with normal tissue—offering a link between NF-κB activation, chronic inflammation and tumor progression.

To investigate the potential for clinical intervention, the authors added a specific NF-κB inhibitor, caffeic acid phenethyl ester (CAPE), to infected gastric carcinoma cells. CAPE treated cells were less viable, produced less IL-1 and IL-8 and demonstrated reduced invasive capacity in a Matrigel assay. CAPE, therefore, has promising therapeutic potential and warrants further investigation for the treatment of gastric cancer.