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Nitric oxide (NO) shows tumoricidal activity. We had previously reportedthat NO downregulates the phosphatidylinositol-3-kinase/Akt pathway, but upregulatesthe MEK/ERK pathway downstream of growth factor signaling. We hypothesized thatNO donor and MEK inhibitor in combination synergistically inhibit the viabilityof cancer cells compared to either NO donor or MEK inhibitor alone. We determinedthe effects of S-nitrosoglutathione (GSNO, NO-donor) and U0126 (MEK inhibitor)on insulin-like growth factor-I (IGF-I) and epidermal growth factor (EGF) signaling,proliferation and invasion in cancer cell lines. GSNO inhibits phosphorylationof IGF-I receptor (IGF-IR), EGF receptor (EGFR) and Akt, but upregulates ERK1/2phosphorylation in MIAPaCa-2 and HCT-116 cells after stimulation by IGF-I andEGF. On the other hand, U0126 inhibits phosphorylation of ERK1/2, but upregulatesphosphorylation of IGF-IR and EGFR in MIAPaCa-2 and HCT-116 cells. The combinationof GSNO and U0126 downregulates phosphorylation of IGF-IR, EGFR, Akt and ERK1/2after stimulation by IGF-I and EGF. GSNO as well as U0126, inhibits the proliferationof MIAPaCa-2, HCT-116, Panc-1, MCF-7, HT-29 and AGS cells in a dose-dependentmanner. GSNO and U0126 in combination synergistically inhibit proliferation andinvasion of cancer cells. These results indicate that the combined treatment ofNO donor and MEK inhibitor may be promising in cancer therapy.

NO donor and MEK inhibitor synergistically inhibit proliferation and invasion of cancer cells