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. 2021 Jan 18;21(3):211. doi: 10.3892/ol.2021.12472

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Copyright: © Sun 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 1. — MCM3AP-AS1-knockdown weakens CDDP resistance in GC cells. (A) The IC₅₀ was tested in NCI-N87, NCI-N87/CDDP, AGS and AGS/CDDP. (B) MCM3AP-AS1 expression in GC cells and CDDP-resistant GC cells was measured by RT-qPCR. (C) The knockdown efficiency of MCM3AP-AS1 in NCI-N87/CDDP and AGS/CDDP cells was assessed by RT-qPCR. (D) Migratory (magnification, ×200) and (E) invasive abilities (magnification, ×200) of CDDP-resistant GC cells were detected after repressing MCM3AP-AS1 by wound healing and Transwell assays, respectively. (F) Cell viability of NCI-N87/CDDP and AGS/CDDP cells was measured after repressing MCM3AP-AS1 by Cell Counting Kit-8 assay. (G) The IC₅₀ of NCI-N87/CDDP and AGS/CDDP was tested after repressing MCM3AP-AS1 by drug-sensitivity assay. *P<0.05 vs. AGS, NCI-N87 or shNC. MCM3AP-AS1, MCM3AP antisense RNA 1; CDDP, cisplatin; GC, gastric cancer; RT-qPCR, reverse transcription-quantitative PCR; sh, short hairpin RNA; NC, negative control; OD, optical density.