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. 2021 Sep 7;24(5):780. doi: 10.3892/mmr.2021.12420

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Copyright: © Lv 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. — The loss of ZSCAN16-AS1 impedes the malignant properties of HCC cells. (A) ZSCAN16-AS1 level in different HCC cell lines was measured by RT-qPCR. (B) HCC cells were silenced by transfection with si-ZSCAN16-AS1, which was confirmed by RT-qPCR. (C) A CCK-8 assay was used to measure the proliferation of ZSCAN16-AS1-silenced HCC cells. (D) Apoptosis of si-ZSCAN16-AS1-transfected HCC cells. Transwell cell (E) migration and (F) invasion assays presented a change in the motility of HCC cells after ZSCAN16-AS1 knockdown (magnification, ×200). (G) HuH7 cells were stably transfected with sh-ZSCAN16-AS1 and then subjected to RT-qPCR analysis to detect the transfection efficacy. (H) Representative pictures show the tumor xenografts. (I) Nude mice were injected with HuH7 cells with stable sh-ZSCAN16-AS1 or sh-NC expression. The growth curves were plotted utilizing the monitored tumor width and length. (J) Weight of the tumor xenografts. **P<0.01. HCC, hepatocellular carcinoma; RT-qPCR, reverse transcription-quantitative PCR; sh, short hairpin; NC, negative control.