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. 2020 May 18;22(2):687–696. doi: 10.3892/mmr.2020.11158

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Copyright: © Zhang 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 4. — SOX4 overexpression reverses NNT-AS1 knockdown-mediated effects on GC cell proliferation, apoptosis, migration and invasion. (A-D) AGS and HGC-27 cells were transfected with sh-NNT-AS1, sh-NC, pcDNA, or NNT-AS1. The mRNA expression levels of SOX4 in (A) HGC-27 and (B) AGS cells. Protein expression levels of SOX4 in (C) HGC-27 and (D) AGS cells. *P<0.05 vs. sh-NC or pcDNA. (E-L) AGS and HGC-27 cells were transfected with sh-NNT-AS1, sh-NC, sh-NNT-AS1 + pcDNA or sh-NNT-AS1 + SOX4. Effect of NNT-AS1 knockdown and SOX4 overexpression on (E) HGC-27 and (F) AGS cell proliferation. Effect of NNT-AS1 knockdown and SOX4 overexpression on (G) HGC-27 and (H) AGS cell apoptosis. Effect of NNT-AS1 knockdown and SOX4 overexpression on (I) HGC-27 and (J) AGS cell migration. Effect of NNT-AS1 knockdown and SOX4 overexpression on (K) HGC-27 and (L) AGS cell invasion. *P<0.05 vs. sh-NC or sh-NNT-AS1 + SOX4. SOX4, sex-determining region Y-related high mobility group box 4; NNT-AS1, nicotinamide nucleotide transhydrogenase-antisense RNA1; GC, gastric cancer; sh, short hairpin RNA; NC, negative control; OD, optical density.