However, there are significant differences in the responses of these fungi to the native defensins and the shorter peptides indicating some degree of specificity in recognition of the c-core motif by each fungus. It is also likely that the shorter peptides derived from native MsDef1 and MtDef4 might have different molecular targets thus leading to varied activity against F. verticillioides and A. flavus. Further studies are needed to unravel the shared as well as unique structure-activity relationships of these two defensins. Gastric cancer is a multifactorial disease, characterized by highly malignant neoplasms in the gastric mucosa, and represents the second leading cause of cancer death worldwide with the highest prevalence in Asia and South America. Environmental associated risk factors include diet, snuff consumption, obesity and Helicobacter pylori infection. Several mutations in tumor-suppressor genes, including P53, adenomatous polyposis coli, E-cadherin and RUNX3, as well as in oncogenes like k-ras, HER2 and b-catenin, have been documented in GC. In addition, over expression of various genes has been documented, including WNT2B, TC1 , and the cyclooxygenase 2 enzyme, which catalyzes the crucial step in the production of prostaglandin E2, a key mediator of joint inflammation. It has been GDC-0199 Bcl-2 inhibitor observed that the expression of the COX2 gene is significantly increased in human gastric adenocarcinoma tissues, when compared with paired gastric mucosal specimens devoid of cancer cells. Such increased expression has been proposed to affect the intensity of invasion, size, lymph node metastases, tumor development and bad prognosis. In this regard, large amounts of data describe chemo-preventive and anticancer activity of non steroidal anti-inflammatory drugs including selective COX2 inhibitors as potential treatments for GC. We initially determined the expression levels of COX2 mRNA in human GC cell-lines MKN45, N87, SNU1, SNU16, KATOIII and AGS, as well as WI38 fibroblasts used here as a control cell line, SAR131675 VEGFR/PDGFR inhibitor examining whether they were correlated with Wnt/b-catenin signaling. As depicted in Figure 1, strong levels of COX2 expression were observed as early as 26 cycles of PCR amplification in metastatic cell lines MKN45, SNU16 and KATOIII, and also in the AGS cell line that is derived from a primary tumor. This result is in agreement with COX2 expression levels detected previously in MKN45, KATOIII and AGS cells. In contrast, COX2 mRNA levels were either very low in WI38 fibroblasts or undetectable in N87 and SNU1 cells, suggesting that this differential pattern of expression is not related to metastatic stages or the level of cell transformation.