Butyrate impairs intestinal tumor cell induced angiogenesis by inhibiting HIF-1α nuclear translocation

increased c-Jun dephosphorylation was not involved. However, an inhibitor of tyrosinespecific phosphatases, orthovanadate, did restore activation-induced phosphorylation of cJun and cytokine production. A correlation ofc-Jun phosphorylation and cytokine production was also seen in T cells derived from cancer patients. Conclusion: Oxidative stress mimicked by hydrogen peroxide treatment inhibited T cell function. This inhibition is at least in part due to a reduction in c-Jun phosphorylation. This effect is mediated by tyrosine phospatase activity and possibly effects upstreamJNK, which requires phosphorylation of its threonin and tyrosine residues to phosphorylate c-Jun. A reduced susceptibility of c-Jun phosphorylation following stimulation was also observed in T cells derived from cancer patients. In accordance with our previous results this data suggests that the cellular immune response in cancer patients is influenced by the redox status of T cells and supports the concept of an antioxidant therapy or a treatment that reduces granulocyte activity.