Results: In 34 cases of gastric cancer, the expression of β-catenin was closed related to the degree of tumor infiltration(γS=0.392 2). The average concentrations of sFas in groups of gastric cancer and control were (380.32+153.08)pg/ml and(23.69+15.38)pg/ml. There was significant difference between two groups(P<0.05). Conclusion: The contents of β-catenin in cell nucleus of gastric cancer tissue and sFas in blood plasma was positively related to the degree of hyperplasia and infiltration of gastric cancer cells. Key Word(s): 1. β-catenin; 2. sFas; 3. Gastric Cancer; Presenting Author: TING LI Additional Authors:

XIAODI ZHAO, YUANYUAN LU, selleck products HANQING GUO, CHANGHAO LIU, HONG LI, LIN ZHOU, YANAN HAN, KAICHUN WU, YONGZHAN NIE, YONGQUAN SHI, DAIMING FAN Corresponding Author: TING LI, YONGQUAN SHI, DAIMING FAN Affiliations: Xijing Hospital of Digestive Diseases; Xijing Hospital of Digestive Diseases Objective: Caudal-related homeobox1 (CDX1), an intestinal specific transcription

www.selleckchem.com/products/Y-27632.html factor, has been reported to play pivotal roles in gastric intestinal metaplasia (IM). Although IM is a high risk factor for gastric cancer (GC), the specific role of CDX1 in GC remains largely unknown. In this study, we investigated the functional roles of CDX1 in GC and its upstream regulatory mechanisms at the microRNA level. Methods: CDX1 expression was detected by immunohistochemistry staining. Bioinformatics analysis and luciferase reporter gene assay were carried to identify the regulating microRNAs. RT-PCR and western blot were adopted to detect the expression of miR-296-5p and CDX1 in GC cell lines and tissues. In vitro and in vivo proliferation selleck chemicals llc assays were performed to study the function of CDX1 and miR-296-5p in gain or loss-of-function model. Western blot were used to investigate

the downstream pathway of CDX1 Results: We found that CDX1 was lost in GC when compared to adjacent IM tissues. Gain-of-function studies showed that CDX1 significantly inhibited GC cell growth by inducing cell cycle arrest and apoptosis. Moreover, we identified miR-296-5p as a direct upstream suppressor of CDX1 and found miR-296-5p is inversely correlated with CDX1 in GC cell lines and clinical samples. miR-296-5p was found to significantly promoted GC cell growth and attenuated the CDX1-induced anti-growth effects by recurring cell cycle distribution and apoptotic status. Furthermore, we found that the ERK1/2 activation and the downstream changes of cell cycle and apoptosis protein levels partly account for the miR-296-5p/CDX1 induced GC growth promotion. We also found that CDX1 may inhibit ERK1/2 activation through suppression of β-catenin transcriptional activity. Conclusion: Our results demonstrated an anti-growth effect of CDX1 and identified its miRNA regulatory mechanism in GC. The identification of this novel miR-296-5p-CDX1-β-catenin-ERK1/2 axis sheds new light on the understanding of the process from IM to GC. Key Word(s): 1. microRNA-296-5p; 2. CDX1; 3.