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. 2019 Jun 7;18(2):1212–1220. doi: 10.3892/etm.2019.7650

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Copyright: © Liu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — miR-16 is involved in SNHG12-mediated colorectal cancer cell proliferation and invasion. SW620 and HT-29 cells were co-transfected with NC siRNA and NC inhibitor (siNC+NC in), NC siRNA and miR-16 inhibitor (siNC+miR-16 in), SNHG12 siRNA and NC inhibitor (siSNHG12+NC in), or with SNHG12 siRNA and miR-16 inhibitor (siSNHG12+miR-16 in). After transfection, (A) reverse transcription-quantitative polymerase chain reaction was used to examine the levels of miR-16. CCK-8 assay using (B) SW620 and (C) HT-29 cells, and (D and E) a Transwell assay (magnification, ×200) were performed to examine cell proliferation and invasion, respectively. **P<0.01 vs. siSNHG12+NC. siSNHG12, siRNA targeting SNHG12; in, inhibitor; SNHG12, small nucleolar RNA host gene 12; siRNA, small interfering RNA; NC, negative control; OD, optical density; miR, microRNA.