Research Paper Volume 13, Issue 1 pp 241—261

Figure 3. In situ self-assembled Au-antimir-155 NCs inhibit HepG2 cell growth. (A, B) Evaluation of gold precursor cytotoxicity in HepG2 and L02 cells using the MTT assay. (C) Dose- and time-response analysis of the effect of different antimiR-155 concentrations on HepG2 viability (MTT assay). (D) Effect of Au-antimiR-155 on endogenous miR-155 expression in HepG2 cells. (E) Flow cytometry analysis of apoptosis in HepG2 cells that generated Au-antimiR-155 NCs or were treated with gold precursor alone (Au NCs). The left and right upper quadrants represent, respectively, early and late apoptotic cells (n=3). (F) Results of MTT proliferation assays in HepG2 cells under different conditions: Inhibitor-NC (inhibitor mimic negative control, 100 nM), in situ synthetized Au NCs (gold precursor, 5 μM), and in situ synthetized Au-antimiR-155 NCs (antimiR-155, 100 nM; gold precursor, 5 μM). (G) Images of wound-healing assays conducted in HepG2 cells under different experimental conditions (100×). Three biological replicates per experiment were assayed. **P<0.01, *P < 0.05.