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. 2020 Oct 29;10:569584. doi: 10.3389/fonc.2020.569584

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Copyright © 2020 Zhang, Yang, Guan, Cheng, Cheng and Wu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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LOXL2 silencing restrained glioma cells amplification, motility, and epithelial-to-mesenchymal transition (EMT) in vitro. U87 (A) and U251 (B) cell amplification slowed after LOXL2 knockdown, measured via colony formation and MTS assays. (C, D) Glioma cells motility decreased following LOXL2 knockdown; scale bar = 100 µm. (E) Western blotting showed that LOXL2 silencing inhibited the expression of cell cycle regulatory protein cyclin D1 and invasion-related proteins MMP-2 and MMP-9. (F) Western blotting showed the regulation of EMT-related proteins after LOXL2 knockdown. (G) Immunofluorescence analysis verified that LOXL2 silencing inhibited the expression of vimentin and N-cadherin; scale bar = 100 µm. **P < 0.01; ***P < 0.005.