• Nasser Ghaly Yousif, Fadhil G Al-Amran, Najah Hadi, Jillen Lee, and Jonthan Adrienne.
• University of Colorado Denver, Department of Medicine and Surgery, 12700 E 19th Avenue, Aurora, CO 80045, USA. yousif_ghaly@yahoo.com
• Cytokine. 2013 Jan 1;61(1):223-7.

BackgroundEsophageal cancer is the seventh leading cause of cancer death in males in USA, and there is a strong link has been demonstrated between inflammation and esophageal cancer, interleukin (IL)-32 is a recently described pro-inflammatory cytokine characterized by the induction of nuclear factor NF-κB activation, the p38MAPK also plays an important role in key cellular processes related to inflammation and cancer. We investigated whether the IL-32 expression may be involved in esophageal carcinogenesis through modulates the activity of NF-κB and p-p38 MAPK.MethodMalignant esophageal tissue and blood samples were obtained from 65 operated untreated patients, normal samples was obtained from 35 patients operated for other reasons as control. IL-32 expression visualized by immunohistochemistry, Real time RT-PCR for IL-32 mRNA expression, NF-κB phosphorylation and phosphorylated p38mapk were analyzed by immunoblotting, ELISA for further detection IL-32 and cytokines (TNF-α, IL-1β, IL-6 and IL-8) concentration in the patient's sera.ResultsIL-32 expression was increased in immunohistochemical staining for malignant esophageal tissue and it's correlated with the relative expression level of IL-32 mRNA P=0.007, the P-NF-κB level elevated in tumor tissue compared with control and no difference in the total NF-κB level P=0.003 while the IL-32 up-regulated the P-pNF-κB in the esophageal tumor P=0.005. There is increase in p-p38MAPK activation underlying IL-32 expression in tumor P=0.004, but no change in total p38 MAPK in malignant esophagus. The plasma level of IL-32 expression was increased in malignant esophageal patients P=0.01, with increased in the levels of the cytokines TNF-α, IL-6, and IL-1βP<0.05.ConclusionsUnderstanding the pathway of IL-32 expression to stimulate the secretion cytokines via the activation of NF-κB and up-regulation of p-p38MAPK may or may not prove to be a therapeutic target, or a biomarker, and future studies will finally answer this hypothesis generated.Published by Elsevier Ltd.

29 keywords...

hide…