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. 2017 Dec 7;15(2):2202–2210. doi: 10.3892/ol.2017.7545

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Copyright: © Han 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 2. — Association between PAK5 and osteosarcoma cell migratory ability. (A) The PAK5 gene was knocked down using Lv-shPAK5 in Saos2 and MG63 cells. The mRNA level of PAK5 and MMP2 was decreased significantly (>75%) in the two cell lines (*P<0.05). No statistically significant difference was identified for E-cadherin, vimentin or fibronectin levels. (B) Western blotting results indicated a marked difference for PAK5 and MMP2 protein expression among these groups. No significant differences were identified for E-cadherin, vimentin and fibronectin. (C) A scratch wound healing assay identified that Lv-shPAK5-transfected Saos2 and MG63 cells exhibited a significantly decreased wound healing rate compared with untreated and Lv-shCon cells. Results are expressed as the mean ± standard deviation. *P<0.05. (D) An in vitro Transwell migration assay identified that PAK5 knockdown attenuated cell migration. The untreated, Lv-shCon and Lv-shPAK5 cells were seeded in the upper Transwell chambers and incubated for 24 h. Images were captured using a light microscope at ×200 magnification of the cells that had migrated into the lower chamber. PAK5, p21-associated kinase 5; Lv-shPAK5, lentivirus-transduced short hairpin RNA targeting PAK5; MMP2, matrix metalloproteinase 2; E-cadherin, epithelial cadherin; Lv-shCon/NC, lentivirus-transduced negative control short hairpin RNA; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; Con, control.