Overall, our results indicated no significant correlation between TNF-α-308G/A polymorphism and increased risk of esophageal cancer in the fixed-effects model (<i>allele model</i>: pooled OR=1.11, 95% CI: 0.96-1.27, <i>homozygote model</i>: pooled OR=1.23, 95% CI: 0.77-1.95, <i>heterozygote model</i>: pooled OR=1.14, 95% CI: 0.97-1.35, <i>dominant model</i>: pooled OR=1.14, 95% CI: 0.97-1.34 and <i>recessive model</i>: pooled OR=1.00, 95% CI: 0.64-1.56).
In this study, we aimed to investigate the clinical significance and biological function of tumor necrosis factor receptor-associated factor 6 (TRAF6) in esophageal cancer.
Preoperative IMD suppressed the elevation of the TNF-α levels after thoracoscopic esophagectomy in patients with esophageal cancer, although no different tendency was detected in terms of IL-6, CRP or postoperative complications.
Taken together, our data indicate that RIPK3 and autocrine production of TNFα contribute to cisplatin sensitivity by initiating necrosis when the apoptotic pathway is suppressed or absent in esophageal cancer cells.
Suppression of tumor necrosis factor receptor-associated protein 1 expression induces inhibition of cell proliferation and tumor growth in human esophageal cancer cells.
The TNF-α-308 gene polymorphism may be significantly associated with the risk of gastric and hepatocellular carcinomas, but not colorectal, pancreatic, or oesophageal cancer, in the Asian population.
In addition, inhibition of PI3K or NFkappaB signaling using the PI3K inhibitor LY294002 or the NFkappaB inhibitor Bay11-7082 increased the sensitivity of Id-1-over-expressing esophageal cancer cells to TNF-alpha-induced apoptosis.