Fig. 3: SNHG17 promotes G1/S transition and cell proliferation.
A The level of phosphorylated-pRb was increased by overexpressing SNHG17 (left panel), but was reduced by silencing SNHG17 (right panel). Cells stably expressing SNHG17 and the control cells (Ctrl) (left panel), or the siRNA-transfected cells (right panel) were subjected to Western blotting. Different exposure times were used to achieve appropriate signal-to-noise for overexpression and knockdown experiments. ppRb, S780-phosphorylated pRb; pRb, total pRb protein. B–C The fraction of cells at the G1-phase was increased by silencing SNHG17 but was reduced by overexpressing SNHG17. NC- or siSNHG17-transfectants (B) and cells stably expressing SNHG17 and the control cells (Ctrl) (C) were synchronized with nocodazole before cell cycle analysis. D–E The serum-stimulated S-phase entry was inhibited by silencing SNHG17 but was promoted by overexpressing SNHG17. NC- or siSNHG17-transfectants (D) and cells stably expressing SNHG17 and the control cells (Ctrl) (E) were serum-deprived and then grown in the 15% FBS-containing medium for the indicated time periods before cell cycle analysis. The percentage of cells at the G1-phase is indicated for each sample. F Silencing SNHG17 inhibited the expression of S-phase genes. NC- or siSNHG17-transfectants were serum-deprived (S-) and then cultured in the 15% FBS-containing medium (S+) for the indicated time periods before qPCR. G–H The fraction of DNA-replicating cells was decreased by silencing SNHG17 but was increased by overexpressing SNHG17. Cells undergoing DNA replication were detected using EdU incorporation assays. For B–C and F–H, error bars represent mean ± SEM from three independent experiments. P values were assessed by unpaired Student’s t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.
