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. 2020 Sep 29;10:544288. doi: 10.3389/fonc.2020.544288

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Copyright © 2020 Guo, Zhang, Li, Lai, Gu, Xu, Chen, Xing, Chen, Qian, Xu, Zeng and Deng.

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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PKM2 promotes EMT, invasion, and migration in prostate cancer cells. DU145 and PC-3 cells were transfected with (A) HA-pcDNA3.1 (HA) control or HA-PKM2 plasmid and (B) scrambled negative control siRNA (siCTL), specific si-PKM2. After transfection for 48h, cell migration and invasion were assessed by Transwell assays. PC-3 was transduced with (C) PKM2 lentivirus (LvshPKM2 or OE-PKM2), or (D) control lentivirus (MOCK or CTL) and expression of epithelial–mesenchymal transition (EMT) markers E-cadherin, N-cadherin, vimentin, matrix metalloproteinase protein (MMP)-9, and MMP-2 were detected by Western blot. (E) Gelatin zymography was used to detect the expression of MMP-2 and MMP-9 in PKM2-overexpressed stable cells lines. Data were representative of three independent experiments and presented as mean ± SD. Values of p were calculated using paired t-test. *p < 0.05, **p < 0.01, ***p < 0.001.