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. 2018 Dec 3;19(2):877–884. doi: 10.3892/mmr.2018.9716

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Copyright: © Li 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. — Effect of ACTL8 on the proliferation of HNSCC PCI-13 cells in vitro. (A) The relative expression of ACTL8 in PCI-13 cells vs. in the normal oral mucosa group. (B) Western blot assay and reverse transcription-quantitative polymerase chain reaction detection were used to evaluate the expression levels of mRNA and protein of ACTL8 following ACTL8 siRNA treatment. Particularly, no significant difference was demonstrated between the blank control (con) and interference control (si-con). (C) At 72 h following ACTL8 siRNA transfection, the viability of PCI-13 cells were measured by a Cell Counting Kit-8 assay by comparing with the si-con group. (D) Plate colony formation assay was conducted to confirm the colony formation rate of PCI-13 cells in si-ACTL8 group and si-con group. Data are presented as the mean ± standard deviation. **P<0.01 vs. si-con. ACTL8, actin-like protein 8; si-ATCL8, small interfering; HNSCC, head and neck squamous cell carcinoma; con, control; OD, optical density.