Fig. 2

miR-129-5p exerts distinct tumor-suppressive functions in vitro and in vivo. A HLE, HLF, Huh7, and HepG2 cells were transfected with 50 nM miR-129-5p mimics. Cell viability was analyzed by WST-1 assay and normalized to miR-control (dotted line). Apoptosis was analyzed by Caspase 3/7 assay and normalized to cell viability and miR-control (dotted line). Data are represented as mean ± SEM. B, C HLE cells were transfected with 50 nM miR-129-5p mimics or miR-control. 48 h after transfection, cell migration (B) was analyzed by transwell assay and expression of CDH1 and VIM (C) was measured by qRT-PCR using the ΔΔCT method. *p < 0.05, **p < 0.01; two-tailed Student’s t test; Scale bar = 200.00 µm. D Huh7 cells were transfected with 50 nM miRNA-129-5p mimics. After 72 h, cells were injected into the flanks of NMRI^nu/nu mice and tumor growth was monitored (n = 7 for each group). Data are represented as mean ± SEM; two-way ANOVA with Šídák’s multiple comparisons test. E HLE, HLF, Huh7, and HepG2 cells were transfected with miR-129-5p mimic. 48 h after transfection, protein expression of p-ERK1/2 and ERK1/2 was analyzed by western blotting with cofilin as loading control; Gels were processed in parallel. Densitometric analysis of western blot assays is shown in Additional file 1: Fig. S9A