Role Of Reactive Oxygen Species

HGF was found to trigger reactive oxygen species (ROS) generation in SCLC. Cigarette smoke generates considerable toxic ROS, which leads to SCLC. ROS play a significant role as signaling molecules in the regulation of various cellular processes, including migration, adhesion, differentiation, and cell growth.76 A recent study by Arakaki et al.77 documented that N-acetylcysteine prevented HGF-suppressed growth of Sarcoma 180 and Meth A cells and HGF-induced apoptosis. In another study, Sattler et al.76 demonstrated that ROS could induce cell cycle progression, increase cell migration, and inhibit protein tyrosine phosphatases that lead to increased phosphorylation of cellular proteins. These studies suggest a link between HGF/SCF-c-Met and ROS in SCLC. They also show that GM-CSF and other growth factors, including IL-3, SF, and TPO, are associated with increased levels of ROS in different hematopoietic cell lines compared with unstimulated cells. PDTC, a broad-range free-radical scavenger, was found to suppress ROS generation as well as GM-CSF-activated signal transduction, suggesting that ROS contribute to growth factor signal transduction.

Very recently, the signaling mechanism of the EGF receptor has been shown to involve generation of H2O2. Goldkorn et al.78 reported H2O2-mediated stimulation of EGF-receptor tyrosine phosphorylation in lung epithelial cells. It was found that in all situations, phosphorylation was somewhat restricted to tyrosine residues. Serine and threonine residues of the EGF receptor were not phosphorylated, and the half-life of the receptor was prolonged after H2O2 exposure. It has been shown that MAP kinase down-regulates EGF-receptor tyrosine kinase activity via phosphorylation of the EGF-receptor Thr669.79

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