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. 2020 Jul 6;22(3):2478–2486. doi: 10.3892/mmr.2020.11302

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Copyright: © Xu 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 3. — RPL32 knockdown inhibits the migration and invasion of SUM 1315 cells. (A) Cell Counting Kit-8 assay indicated that 1315-KD cells had a similar proliferative ability compared with 1315-CON cells. (B) Wound-healing assay (magnification, ×100) demonstrated that RPL32-silenced cells (C) exhibited a delayed wound closure of scratch gaps, compared with the control cells. (D) Transwell assays revealed that (E) fewer 1315-KD cells than 1315-CON cells invaded the filter, with or without Matrigel. 1315-CON and SUM 1315 cells were stably transfected with negative control lentivirus. 1315-KD and SUM 1315 cells were stably transfected with RPL32 siRNA lentivirus. Scale bar, 200 µm. *P<0.05 vs. 1315-CON cells. RPL32, ribosomal protein L32; si, small interfering; CON, control; OD, optical density; KD, knockdown.