That β-catenin failed to combine with TCF4 and the following inhibitory expression of their downstream factors might play a key role in the decrease of invasion and proliferation ability of SGC-7901 cell in vivo and in vitro as showed above. Conclusion: This study demonstrates that FH535 can inhibit proliferation and invasion

selleck products of human gastric adenocarcinoma cell line SGC-7901 in vivo and in vitro. Further, these phenomena may relate to the lower expression of c-Myc and cyclin-D1. Key Word(s): 1. FH535; 2. gastric neopasia; 3. cell prolifration; 4. cell invation; Presenting Author: YING SHAO Additional Authors: SHENG-TAO ZHU, PENG LI, YONG-JUN WANG, YONG-DONG WU, BANG-WEI CAO, SHU-TIAN ZHANG Corresponding Author: YING SHAO Affiliations: Friendship Hospital, Capital Medical University; Friendship Hospital, Capital medical

University; Friendship Hospital, Captital Medical University Objective: Overexpression of cyclooxygenase-2 (COX-2) is associated with the carcinogenesis of esophageal squamous cell carcinoma (ESCC). Bioinformatic analysis showed that miR-26a and miR-144 could bind to 3′ UTR of COX-2. In this study, we planned to investigate the functions and mechanisms of two miRNAs in ESCC. Methods: Eleven ESCC cell lines, one immotalized esophageal cell (Het-1A), 30 pairs ESCC and corresponding non-tumour tissues, and BALB/c nude mice were selected to study. Real-time PCR was used for detecting miRNAs in tissue samples and cell lines, western blot for COX-2 protein in cell lines. CCK8, transwell chamber assay and flow cytometry were used to Crizotinib chemical structure detect the functional change of ESCC cell lines after being overexpressed these miRNAs by constructing stable over-expression clones. Dual luciference reporter gene assay were used to verify that miR-26a and miR-144 could target COX-2 in ESCC. ESCC cell lines that were stably transfected with miR-26a, miR-144 and miR-26a-144 were injected into subcutaneous or tail veil of nude mice. 上海皓元 The

volume of tumour or numbers of tumour nodules formed on the liver surfaces were calculated. Results: The expression level of two miRNAs were down-regμlated in both ESCC cell lines and ESCC tissues. MiR-26a and miR-144 could inhibit the metastasis of ESCC both in vivo and in vitro. Cluster vector of miR-26a and miR-144 could enhance the inhibitive metastasis effect of miR-26a or miR-144 and had inhibitive proliferation effect on ESCC, while miR-144 or 26a did not have inhibitive effect on proliferation in ESCC. The inhibitive effect of miR-26a and miR-144 on ESCC was partly through COX-2 pathway. Conclusion: MiR-26a and miR-144 could inhibit the development and progression of ESCC through inhibiting COX-2 pathway. MiR-26a and miR-144 had better inhibitive effect on the development and progression of ESCC by constructing cluster vector of miR-144 and miR-26a. Key Word(s): 1. ESCC; 2. Cyclooxygenase-2; 3. miR-26a; 4.