G) The mRNA and ( H, I) protein levels of CCND1 were determined by Real-Time qPCR and Western Blot analysis, respectively. (Note: “Con” indicated “Control”, “KD-L” indicated “Knock-down of LncRNA SNHG16” and “KD-L+KD-miR” suggested “both LncRNA SNHG16 and miR-17-5p ablation”). Each experiment repeated at least 3 times, and * P 0.05. Knock-Down of LncRNA SNHG16 Inhibited OSCC Progression Through the miR-17-5p/CCND1 Axis We next investigated whether LncRNA SNHG16 regulated OSCC development by targeting the miR-17-5p/CCND1 axis. To achieve this, the LncRNA SNHG16 silencing vectors, miR-17-5p inhibitor and CCND1 overexpression vectors were delivered into OSCC cells (Figure 6A and B), which were divided into four groups, including Control, KD-SNHG16, KD-SNHG16+miR-17-5p inhibitor, and KD-SNHG16+OE-CCND1. As expected, the data in Figure 6C and D showed that knock-down of LncRNA SNHG16 inhibited cell proliferation in OSCC cells, which were restored by silencing miR-17-5p and upregulating CCND1. Consistently, the promoting effects of LncRNA SNHG16 ablation on cell apoptosis were also abrogated by miR-17-5p downregulation and CCND1 overexpression (Figure 6E and F). Next, by performing Western Blot analysis, we noticed that both miR-17-5p ablation and CCND1 overexpression restored the expressions of N-cadherin and Vimentin in LncRNA SNHG16-deficient OSCC cells, resulting in the promotion of EMT (Figure 7A–D).