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. 2020 Jul 10;44(3):1064–1074. doi: 10.3892/or.2020.7684

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Copyright: © Chang 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. — TTN-AS1 accelerates glioma cell viability, migration and invasion, as well as inhibits apoptosis in vitro. (A) Glioma U251 and LN229 cells were transfected with TTN-AS1 knockdown oligonucleotides (si-TTN-AS1-1 and si-TTN-AS1-2) or control (sh-ctrl) and the relative TTN-AS1 level was assessed. (B) CCK-8 assays displayed the viability of glioma cells following silencing. (C) Flow cytometry assays demonstrated the apoptotic state of the glioma cells following silencing of TTN-AS1. (D) Wound healing assays presented the migration ability of the glioma cells following silencing of TTN-AS1. (E) Transwell assays presented the invasion ability of the glioma cells following silencing of TTN-AS1. **P<0.01, compared with the si-ctrl group. TTN-AS1, long non-coding (lnc)RNA titin-antisense RNA1.