Figure 2

MiR-216b suppresses cell proliferation both in vitro and in vivo. (a) MiR-216b expression is lowest in HepG2 cells and highest in SMCC-7721 cells. (b) The mimics and inhibitors of miR-216b could significantly affect the expression of miR-216b and the negative control RNAs (NC) had no obvious effect on expression of miR-216b. (c) By CCK-8 assay, the miR-216b upregulated HepG2 cells have smaller value than control cells and Wild Type (WT) cells, and miR-216b downregulated SMCC-7721 cells have larger value than control cells and WT cells. (d) Soft agar colony formation assay shows the suppression role of miR-216b in HCC cells’ proliferation. (e and f) MiR-216b attenuated HCC tumor growth in mouse xenograft models. The left panels show tumor formation upon subcutaneous injection of HepG2 cells that were continually transfected with the miR-216b mimics or control vector into nude mice. The right panels show tumor formation upon transplantation of SMCC-7721 cells was continually transfected with the miR-216b inhibitor or control vector into nude mice. (g) Flow cytometry study indicating the apoptotic rates in miR-216b overexpressing cells and control cells. MiR-216b induced apoptosis by regulating the important factors of the extrinsic apoptotic pathway