Fig. 4: SNHG17 promotes tumor cell growth via c-Myc.

A–B The cell growth was inhibited by silencing SNHG17 but was promoted by overexpressing SNHG17. NC- or siSNHG17-transfectants (A) and cells stably expressing SNHG17 and the control cells (Ctrl) (B) were subjected to cell counting assays. C–D The colony formation of hepatoma cells was suppressed by silencing SNHG17 but was promoted by overexpressing SNHG17. E The tumor growth was promoted by overexpressing SNHG17 in vivo. HCCLM9 cells stably expressing SNHG17 and the control cells (Ctrl) were subcutaneously injected into NCG mice (n = 5). F Ectopic expression of c-Myc antagonized the roles of siSNHG17 in decreasing DNA-replicating cells (left panel) and cell growth (right panel). Cells stably expressing c-Myc and the control cells (Ctrl) were co-transfected with the indicated siRNA duplex and then subjected to EdU incorporation assays (left panel) or cell counting (right panel). G Silencing c-Myc abrogated the roles of SNHG17 in increasing DNA-replicating cells (left panel) and cell growth (right panel). Cells stably expressing SNHG17 and the control cells (Ctrl) were co-transfected with the indicated siRNA duplex and then subjected to EdU incorporation assays (left panel) or cell counting (right panel). For A–D and F–G, error bars represent mean ± SEM from three independent experiments. P values were assessed by unpaired Student’s t test (A–D; E, right; F–G), or two-way ANOVA (E, left). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.