Survivin antisense compound inhibits proliferation and promotes apoptosis in liver cancer cells

Figure 1 Generation and optimization of antisense compound. Each value represents the mean±SD of three independent experiments.

Figure 2 Survivin expression level (mRNA and protein) in HepG₂ cells treated with antisense compound (1:4). A: Sensitivity of survivin mRNA in RT-PCR assay; B: Level of survivin mRNA expression in HePG₂; C and D: Western blot analysis of survivin protein expression in HePG₂ cells.

Figure 3 Effect of antisense compound (1:4) on the growth and viability of HepG₂ cells. A: Cells incubated with an increasing concentration of antisense compound (1:4), 600 nmol/L sense compound (1:4), 600 nmol/L LiP, or 600 nmol/L (ODNs) for 48-h after the start of transfection; B: untreated cells; C-E: photomicrographs of HepG₂ cells after a 48-h transfection with (C) 600 nmol/L antisense comound (1:4), (D) 600 nmol/L sense compound (1:4) or (E) 600 nmol/L LiP.

Figure 4 Anti-active caspase-3 antibodies for measuring apoptosis by flow cytometric analysis.

Figure 5 Morphological evaluation of HepG₂ cells(original magnification, ×4000). A: Normal structure in the nuclei and cytoplasm of untreated cell; B: Morphological changes of apoptosis in treated cells.

Figure 6 Laser scanning confocal microscopy of localization of survivin protein in HepG₂ cells. A: Expression and localization of endogenous survivin proteins with immunofluorescence analysis of untreated cells by using the polyclonal anti-survivin antibody and FITC-labeled anti-rabbit-IgG as secondary antibody; B: Rare and weakly stained cells treated with antisense compound inside the cytoplasm and morphological changes corresponding to apoptosis.