The present study was aimed to investigate the effect of miR-107 transfection on gastric cancer cell growth. Results from qRT-PCR revealed that level of miR-107 in SGC-7901 and MKN1 cell lines was down-regulated in comparison to the normal cells, GES-1. CCK-8 assay revealed a significant reduction in the proliferation of SGC-7901 cells on transfection with miR-107. The tumor growth was very slow in the mice implanted with SGC-7901/miR-107 compared to those bearing SGC-7901/miR-NC. In SGC-7901 cells metastasis potential after miR-107 transfection was examined using wound-healing and Transwell invasion assays. The migration as well as invasion potential of SGC-7901 cells was significantly lower on transfection with miR-107. The activity of luciferase was reduced markedly in SGC-7901 cells co-transfected with miR-107 mimic compared to miR-NC. However, miR-107 mimic co-transfection did not affect the luciferase activity in SGC-7901 cells bearing mutant-type BDNF 3'UTR. Western blot assay showed that miR-107 overexpression causes inhibition of BDNF mRNA and protein expression in SGC-7901 cells. The CCK8 assay showed that pBDNF transfection prevented miR-107 mediated inhibition of SGC-7901 cell proliferation. miR-107 mimic transfection inhibited expression of BDNF and activation of PI3K (p-PI3K) and AKT (p-AKT) in SGC-7901 cells. In order to confirm whether activation of PI3K and AKT by miR-107 mimic involves inhibition of BDNF, the cells were co-transfected with si-BDNF. The results revealed that si-BDNF transfection led to inhibition of BDNF expression and PI3K and AKT activation in SGC-7901 cells. In summary, the present study demonstrates that miR-107 expression inhibits proliferation and metastasis in gastric cancer cells. Therefore, miR-107 acts as tumor inhibitor for gastric cancer through targeting BDNF expression. Thus miR-107 can be used for treatment of gastric cancer.
Keywords: Luciferase activity; Metastasis; Transfection; Transwell invasion; Wound-healing.
Copyright © 2018 Elsevier Ltd. All rights reserved.