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Báo cáo y học: "miR-223 regulates migration and invasion by targeting Artemin in human esophageal carcinoma"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: miR-223 regulates migration and invasion by targeting Artemin in human esophageal carcinoma | Li et al. Journal of Biomedical Science 2011 18 24 http www.jbiomedsci.eom content 18 1 24 NSC The cost of publication in Journal of Biomedical Science Is borne by the National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access miR-223 regulates migration and invasion by targeting Artemin in human esophageal carcinoma 1 1 t I- z 1 1 1 2 7 I- 1 1 Shujun Li Zhigang Li Fengjie Guo Xuebo Qin Bin Liu Zhe Lei Zuoqing Song Liya Sun Hong-Tao Zhang 2 Jiacong You1 and Qinghua Zhou1 Abstract Background Artemin ARTN is a neurotrophic factor belonging to the glial cell-derived neurotrophic factor family of ligands. To develop potential therapy targeting ARTN we studied the roles of miR-223 in the migration and invasion of human esophageal carcinoma. Methods ARTN expression levels were detected in esophageal carcinoma cell lines KYSE-150 KYSE-510 EC-9706 TE13 esophageal cancer tissues and paired non-cancerous tissues by Western blot. Artemin siRNA expression vectors were constructed to knockdown of artemin expression mitigated migration and invasiveness in KYSE150 cells. Monolayer wound healing assay and Transwell invasion assay were applied to observe cancer cell migration and invasion. The relative levels of expression were quantified by real-time quantitative PCR. Results ARTN expression levels were higher in esophageal carcinoma tissue than in the adjacent tissue and was differentially expressed in various esophageal carcinoma cell lines. ARTN mRNA contains a binding site for miR-223 in the 3 UTR. Co-transfection of a mir-223 expression vector with pMIR-ARTN led to the reduced activity of luciferase in a dual-luciferase reporter gene assay suggesting that ARTN is a target gene of miR-223. Overexpression of miR-223 decreased expression of ARTN in KYSE150 cells while silencing miR-223 increased expression of ARTN in EC9706 cells. Furthermore overexpression of miR-223 in KYSE150 cells decreased cell migration and invasion. Silencing of miR-223 in EC9706 .