Abstract: To investigate the effect of microRNA-138 ( miR-138 ) on the proliferation of the human gastric cancer cell line SGC-7901 and its possible mechanism. Methods: miR-138 RNA was transfected into the human gastric cancer cell line SGC-7901 using Lipofectamine2000. The expression level of miR-138 before and after the transfection was measured by real time PCR ( RT-qPCR ) to observe the effect of transfection on the abundance of miR-138 expression in the SGC-7901 cells. After transfection the cell cycle was examined by flow cytometry. The growth curve was measured with MTT to observe the change in cell proliferation after an induced upregulation of miR-138 expression. Furthermore, Western blot was conducted to detect the expression of the human telomerase reverse transcriptase ( hTERT ) protein as a preliminary probe of the possible mechanism. Results: miR-138 was transfected into SGC-7901 effectively by Lipofectamine2000, with a transfection rate of nearly 100%. The upregulation of miR-138 expression in SGC-7901 cells after the miR-138 RNA transfection amounted to 7.51 times that in the cells of the control group ( P < 0.05). The results of flow cytometry showed that the proliferation index ( PI ) of the SGC-7901 cells without transfection was 36.72.  However, the PI value of the SGC-7901 cell line significantly decreased to 24.52 after the cells were transfected with miR-138 RNA. The MTT results also showed that there was a significant decrease in the capacity of SGC-7901 proliferation after miR-138 RNA transfection ( P < 0.05 ). Western blot results showed that the expression of hTERT protein in SGC-7901 cells after transfection was down-regulated, but this expression was still enough to be detected. The expression of hTERT protein remained mostly unchanged in the SGC-7901 cells transfected with negative control RNA. Conclusion: miR-138 RNA can effectively suppress the proliferation of human gastric cancer cell line SGC-7901, and suppressing protein expression of its target gene hTERT may possibly be the mechanism.