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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 silenci

Eteläuomen läiUnited statesCorning coCentral south universityChinese academy of sciences shanghaiLife technologyCell bankAnimal centerXiangya medical collegeCentral south university noHaikou hospital of xiangya medical collegeAffiliated haikou hospitalCentral southWestern blotEthics committeeAmerican type culture collection