ObjectiveTo analyze the expression of Hsa-miR-29c in gastric cancer and its mechanism of action, and to explore its relationship with clinicopathological characteristics and prognosis of gastric cancer patients.MethodsTheoverexpression of Hsa-miR-29c in gastric cancer cell lines of MKN28 and MKN45 were established by lentivirus transfection (transfection group), and the control group of empty lentivirus (negative control group) was established. The expressions of Hsa-miR-29c in cells of the two groups after transfection were detected by real time polymerase chain reaction (qRT-PCR), and the proliferation and clonogenesis of cells in the two groups were detected by CCK-8 and plate cloning. The expression of extracellular matrix protein 1 (ECM1), type Ⅰ collagen (Col Ⅰ), smooth muscle actin(α-SMA), matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the two groups were detected by Western blot. qRT-PCR and immunohistochemistry were used to detect the expression of Hsa-miR-29c in 70 gastric cancer tissues and adjacent tissues respectively, and then analyzed its relationship with the clinicopathological features and prognosis of gastric cancer.ResultsThe stable expression of Hsa-miR-29c gastric cancer cell line was successfully constructed in this research, the expression of Hsa-miR-29c in the transfection group was significantly higher than that in the negative control group (P<0.05). The proliferation and clone forming ability of MKN28 and MKN45 cells in the transfection group were significantly lower than those in the negative control group (P<0.05). Compared with the negative control group, the expression of Col Ⅰ and TIMP-1 in MKN28 and MKN45 cells were increased after transfection, while the expression levels of ECM1, α-SMA, and MMP-2 were significantly decreased, with significant differences between the two groups (P<0.05). The expression level of Hsa-miR-29c in gastric cancer tissues was significantly lower than that of adjacent tissues (P<0.05), and the positive expression rate was not related to age, sex, and pathological type (P>0.05), but related to tumor size, TNM stage, tumor differentiation, and lymph node metastasis (P<0.05). The mean survival time (MST) of patients with negative expression of Hsa-miR-29c was significantly shorter than that of patients with positive expression (P=0.029).ConclusionsHsa-miR-29c is down expressed in gastric cancer, and is related to the clinical characteristics and prognosis of it. The overexpression of Hsa-miR-29c can inhibit the proliferation of gastric cancer cells, and the mechanism may be related to the inhibition of extracellular matrix (ECM) signaling pathway.