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. 2016 Feb 10;16(4):497–511. doi: 10.1177/1533034616630866

Figure 5.

Figure 5.

miR-139 inhibited Akt, MAPK, and c-Myc signaling through insulin-like growth factor type 1 receptor (IGF-1 R) and associate of Myc-1 (AMY-1). A and B, U87MG and U251 cells were transfected with IGF-1 R or miR-139 and empty vector or scramble as negative controls. The protein expression of downstream signaling was detected (n = 4). C, Insulin-like growth factor type 1 receptor was transfected into miR-139 overexpressing U87MG cells and the total and phosphorylation level of Akt and MAPK were detected (n = 3). D, The glioma cells were overexpressing IGF-1 R and added with Akt inhibitor at the same time. The peroxisome proliferator-activated receptor γ coactivator 1β (PGC-1β) expression was detected (n = 4). E, The glioma cells were transfected with AMY-1 or miR-139 and the expression level of c-Myc signaling molecules was evaluated (n = 4). F, AMY-1 was transfected into miR-139 overexpressing U87MG cells and the RNA levels of cell division cycle 25 homologue A (cdc25A) and p27 were detected (n = 3). Bars represent means ± SD, *P < .05, **P < .01, ***P < .001.