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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Gastrin inhibits gastric cancer progression through activating the ERK-P65-miR23a/27a/24 axis

Fig. 6

Gastrin inhibited GC cell proliferation through activating the ERK-P65-miR23a/27a/24 axis in vitro. The p-ERK, p-P65 (a), and miR-23a, miR-27a, and miR-24 (b) levels were increased and cyclin D1 levels and proliferation of SGC7901 cells (c) were decreased after gastrin treatment. SGC7901 cells were treated with 10− 7 mol/L gastrin for indicated duration. The p-ERK, p-P65, and cyclin D1 levels were determined using Western blotting. MicroRNA levels were determined by qRT-PCR and normalized to U6. The fold change was calculated using the 2−ΔΔCt method. Proliferation of SGC7901 cells were determined by living cell counting. d Sequence alignment between cyclin D1 (CCND1) 3’ UTR and miR-23a, miR-27a, and miR-24 using Vector NTI 6.0 software. e The miR-23a, miR-24, and miR-27a mimics suppressed luciferase activity ofCCND1 3′-UTR reporter gene after cotransfectionin to HEK293T cells. Renilla luciferase reporter gene was used as normalization control for transfection efficiency. *, compared with the control group, p<0.05. All experiments were repeated three times

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