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5-Florouracil (5-FU) is the basic agent used in the treatment of gastric cancer. Capecitabine, a prodrug of 5-FU, displays increased antitumor efficacy compared with 5-FU in the clinic. 5′-Deoxy-5-fluorouracil (5′-DFUR), the metabolite of capecitabine, is converted to 5-FU by the enzyme thymidine phosphorylase (TP), which is present at high concentrations in human tumors. In this study, we investigated the effect of interferon-  α   (IFN-  α  ) on the sensitivity of gastric cancer cells to treatment with 5′-DFUR and its relationship with TP expression. Preincubation of gastric cancer cells with IFN-  α   enhanced 5′-DFUR-induced apoptosis via IFN-  α  -mediated upregulation of TP. The depletion of TP with small interfering RNA (siRNA) obviously inhibited IFN-  α  -induced upregulation of TP expression and thus prevented apoptosis induced by IFN-  α   and 5′-DFUR. Treatment with IFN-  α   and combined IFN-  α   and 5′-DFUR treatment were also associated with concomitant activation of ERK signaling. Treatment with the ERK inhibitor PD98059 or depletion of ERK with siRNA partially reversed IFN-  α  -induced upregulation of TP expression, thus partially preventing apoptosis induced by IFN-  α   and 5′-DFUR. Taken together, our study shows that IFN-  α   enhanced 5′-DFUR-induced apoptosis in gastric cancer cells by upregulation of TP expression, which is partially regulated by activation of ERK signaling.

Interferon-αEnhances 5′-Deoxy-5-Fluorouridine-Induced Apoptosis by ERK-Dependant Upregulation of Thymidine Phosphorylase