Figure 2. MiR-27a-3p acted as a tumor suppressor gene in HCC.

HepG2 cells were chosen for miR-27a-3p overexpression and PLC cells were selected for miR-27a-3p knockdown. (A,B) MTT assays showed that high level of miR-27a-3p impaired the cell viability in HepG2, whereas its low level added viability in PLC. (C,D) Up-regulation of miR-27a-3p increased the apoptosis rate in HepG2. In contrast, knockdown of miR-27a-3p significantly reduced the apoptosis rate in PLC. (E,F) The cell cycle assays revealed that overexpression of miR-27a-3p led to an increase in G₀/G₁ phase and a decrease in S-phase in HepG2, while its knockdown resulted in a reverse trend in PLC. All experiments were performed in triplicate. *P<0.05.