The present study demonstrated Caspase 3 that NAC suppresses the activation effect of nicotine on the expression of uPAR. In addition, exogenous ROS induces only the expression and Promotoraktivit t of uPAR. Several laboratories have reported convincing evidence, that provides protection against the penetration of antioxidants and tumor metastasis in vivo and in vitro. Asc 2 O 6 Ophosphate palmitate, a lipophilic derivative flammable and self-oxidation of ascorbic Acid contains LT, The penetration of fibrosarcoma cells inhibits using its antioxidant activity T. Exogenous ROS by the xanthine oxidase hypoxanthine systemcan the immigration of mesothelial cells generated. Our results agree with previous reports on the r The NF and AP-1 in uPAR expression by Lithochols Acid in cancer cells, c Lon and F Promotion protein in macrophages AGS gastric cancer cells. The transcription factor AP 1 by MAPK in Dependence Of different cell types and stimuli regulate. The transcription of c-fos and c is June improved through active MAPK. Make transcriptionally, C activity in June T by phosphorylation of Transkriptionsaktivierungsdom Ne potentiated by JNK. In this context, an AP-activity of t determined by the abundance of an AP subunit c-fos and c June nicotine-induced c-fos and c-June expression in our system. In addition, the inhibitory effect of PD98059 and SP600125 induced on nicotine an AP activity t, suggesting that upstream signaling to the transcription factor AP-1 was Erk 1/2 and JNK. The inhibition of NF dependent Independent transcription NAC, a free-radical singer, and its activation by exogenous H2O2 noted that ROS are signaling molecules upstream rts to NF . Li and Engelhardt reported that the recruitment of NIK to TRAF6 essential for mechanically induced activation of NF ROS . Storz and Toker has shown that the protein kinase D essential for ROS-induced activation of NF by induction of tyrosine phosphorylation of IKK. Src and abl mediation PKDactivation toH2O2 stimulation in response, through phosphorylation of Tyr463 in the PKD pleckstrin homology Cathedral sharing plans. In Similar way, Fan et al. reported that ROS controlled EAA activation of NF Src tyrosine phosphorylation of c to I h Depends . However, ROS-induced activation of NF is heavily dependent Ngig the cell type. Together, in the present study, the first time on the R Of nicotine in the regulation of uPAR and the Invasivit t of human cells in ECV304 endothelial cells. Our study suggests that MAPK and ROS by nicotine stimulates AP 1 and NF or uPAR expression and increased thereafter Hte Invasivit t of ECV304 cells upregulated loan St. Ren conflict of interest The authors explained That no conflict of interest. Acknowledgements We are grateful to Dr. Y.Wang for uPAR promoter reporter construct, Dr. N. Ahn theMEK for construction, Dr. MJ Birrer for June, v. Dr. DW Ballard for the I and IBuild and WC Streptozotocin Greene for NIK construct. This work was funded by a research grant from the National Cancer Center, a Science Research Foundation of Basic Research Program through the National Beh Rde by the Korean Ministry of Education, Science and Technology and supported by a Medicalcharacteristics of obesity. We have shown that stretching has cell inhibitory eff.