Objective:To investigate the possible role of miR-145 in the formation of cisplatin resistance in human gastric cancer cell line. Methods:Expression of miR-145 was assayed by quantitative real-time PCR. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide) and clonogenic assays were used to detect cell viability and the drug-resistance phenotype changes of-cancer-cells associated with up-regulation or down-regulation of miR-145. Dual-luciferase activity assay was used to testify the target genes of miR-145. Protein expressions were measured by western blot,immunohistochemistry or Immunofluorescence staining. Flow cytometry was used to detect CDDP induced apoptosis. Results:We found that miR-145 was significantly down-regulated in both gastric cancer tissues and various gastric cancer cell lines. In addition,it was down-regulated in cisplatin-resistant gastric cancer cell line SGC7901/cisplatin (DDP) and the down-regulation of miR-145 was concurrent with the up-regulation of IGF1R and IRS1,compared with the parental SGC7901 cell line,respectively. In vitro drug sensitivity assay demonstrated that over-expression of miR-145 sensitized SGC7901/DDP cells to cisplatin. The luciferase activity of the above proteins 3＇-untranslated region-based reporters constructed respectively in SGC7901/DDP cells suggested that IGF1R and IRS1 were the direct target genes of miR-145. Enforced miR-145 expression reduced its target proteins level,inhibited SGC7901/DDP cells proliferation and enhanced SGC7901/DDP cells to DDP-induced apoptosis. Conclusion:Our findings suggested that hsa-miR-145 could modulate cisplatin resistance of human gastric cancer cell line at least in part by targeting IGF1R and IRS1.