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. 2019 Jun 7;17:455–464. doi: 10.1016/j.omtn.2019.04.030

Figure 6.

Figure 6

AMPK Was a Direct Target of miR-101-3p

(A) The CCK-8 assay showed that MKN28 cells transfected with miR-101-3p inhibitor grew at a dramatically higher rate as compared with controls. (B) CCK-8 assay showed that miR-101-3p overexpression markedly inhibits the cell growth of BGC823 cells when compared with cells transfected with miR-nc. Error bars represent mean ± SD from three independent experiments. **p < 0.01. (C) miR-101-3p is highly conserved across species and binding sites within the seed region sequence in the 3′ UTR of AMPK. (D) Luciferase assay in HEK293 cells. pmirGLOI-AMPK-WT or pmirGLO-AMPK-MUT vector was co-transfected with miR-101-3p vector. Luciferase activity in pmirGLOI-AMPK-WT group denoted a statistically significant decrease following ectopic expression of miR-101-3p. (E) Transfection of the miR-101-3p inhibitor increased the expression of AMPK in BGC823 cells. All tests were performed at least three times. Data were expressed as mean ± SD. **p < 0.01.