This study is designed to evaluate the effects of UA and NS398 on COX-2 negative gastric cancer cell line MGC-803, which is in an attempt to develop potent antitumor agents. Methods: To investigate the effects of UA and

COX-2 inhibitor NS398 on the proliferation of COX-2 positive gastric cancer cell line SGC-7901 and COX-2 negative gastric cancer cell line MGC-803.Methods: SGC-7901 cells and MGC-803 cells were seeded in RPMI-1640 supplemented with 10% heat-inactivated fetal calf serum and routinely incubated for 24h. After serum-free starvation for 24h, the cells were cultured with either UA at the Final concentration of 10, 20, 40, 80 μmol/L or NS-398 at the final concentration of RXDX-106 50, 100, 200, 400 μmol/L for 12, 24 and 48h respectively. Cell proliferation was determined using

methyl thiazolyl tetrazolium (MTT) colorimetric assay. Results: Both UA and NS398 significantly inhibited SGC-7901 and MGC-803 cell proliferation in a dose- and time-dependent manner. Conclusion: Both UA and COX-2 inhibitor NS398 significantly inhibited cell proliferation of COX-2 Protein Tyrosine Kinase inhibitor positive gastric cancer cell line SGC-7901 and COX-2 negative gastric cancer cell line MGC-803. Key Word(s): 1. gastric cancer; 2. Ursolic acid; 3. NS398; 4. proliferation; Presenting Florfenicol Author: NADIR ARBER Additional Authors: SHIRAN SHAPIRA, ASSAF SHAPIRA, DINA KAZANOV,

SARAH KRAUS Corresponding Author: SHIRAN SHAPIRA, DINA KAZANOV, NADIR ARBER, SARAH KRAUS Affiliations: sourasky medical center, Tel Aviv University Objective: Background: K-Ras mutations are present in 95% of pancreatic cancer (PC) cases. We propose a “Troyan Horse” approach which exploits this pathway. We have previously shown that adenovirus, carrying the pro-apoptotic PUMA gene, regulated by Ets and AP1/Ras- responsive elements (RREs; Py2-SV40-PUMA), suppressed the growth of Ras-mutated cancer cells. Additional vectors; Py4-; Py5-SV40-PUMA containing several RREs repeats, were effective in selectively targeting Ras-mutated tumor cells. We utilized a MazE-MazF (MazEF) unique toxin-antitoxin (TA) system encoded from the E. coli genome. Under silent conditions the antitoxin inhibits the toxin and the toxin-antidote complex represses the TA operon, whereas after activation, proteolytic antitoxin degradation outpaces its synthesis. Aim: Improve vectors’ therapeutic efficacy and specificity by substituting the lethal gene with highly regulated toxic agents.