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【目的】探讨miR-143在膀胱癌组织中的作用及机制，为膀胱癌的临床诊治提供参考。【方法】选用体外培养的T24细胞株作为研究对象，按照处理方式分为si-COX-2转染组、miRNA-143转染组、阴性对照组、空白对照组。Transwell趋化实验和3 H-thymidine 法检测 T24细胞增殖和迁移能力，免疫印迹法检测COX-2蛋白表达变化。【结果】miR-143和si-COX-2转染T24细胞48～72 h后，细胞增殖能力较正常T24细胞相比下降36％～49％（ P ＜0．01），迁移能力下降81％。免疫印迹结果表明，si-COX-2或miR-143转染的T24细胞内源性COX-2表达水平显著减少至正常T24细胞表达水平的0．39和0．31倍（ P＜0．01）。【结论】miR-143可能通过COX-2通路发挥对膀胱癌 T24细胞的增殖和侵袭的抑制作用并抑制COX-2的表达。提示miR-143可作为膀胱癌的治疗候选药物。“,”[Objective] To explore the role of miR-143 in bladder cancer tissue and its mechanism in order to provide the reference for clinical diagnosis and treatment of bladder cancer .[Methods]T24 cell strains in vitro were chosen .According to the treatment methods ,T24 cells were divided into si-COX-2 transfection group ,miR-143 transfection group ,negative control group and blank control group .The proliferation and mi-gration of T24 cells was examined by Transwell chemotaxis assay and 3 H-thymidine method ,respectively .The expression level of COX-2 was determined by Western blotting .[Results] Compared with normal T24 cells , the cell proliferation ability of T24 cells after transfection with miR-143 and si-COX-2 for 48~72h decreased by 36% ~49% ( P <0 .01) ,and the migration ability decreased by 81% .Immunoblotting results showed that the expression of endogenous COX-2 in T24 cells after transfection with si-COX-2 or miR-143 significantly de-creased to 0 .39 and 0 .31 times of that in normal T24 cells( P <0 .01) .[Conclusion] The miR-143 may play the role in inhibiting the proliferation and invasion of T 24cells and the expression of COX-2 through COX-2 pathway ,which indicates that miR-143 can be used as the candidate therapeutic agent for bladder cancer .