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. 2019 Jul 30;42(4):1283–1294. doi: 10.3892/or.2019.7254

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Copyright: © Niu 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 5. — Potential involvement of CPXM2 in the regulation of EMT. (A) GSEA enrichment plots indicate that CPXM2 expression was positively correlated with apical junction and EMT gene signatures. High CPXM2 expression in GC patients was positively correlated with the (a) HALLMARK_APICAL_JUNCTION and (b) HALLMARK_EPITHELIAL_MESENCHYMAL_TRANSITION gene sets. (B) CPXM2 was significantly correlated with several key genes associated with EMT: (a) SNAI1, (b) TWIST1, (c) ZEB1, (d) vimentin, (e) E-cadherin and (f) N-cadherin. (C) Western blotting analysis was used to compare expression of epithelial and mesenchymal markers between GC cells infected with shCPXM2 or scramble. GAPDH was used as loading control. CPXM2, carboxypeptidase X, M14 family member 2; FDR, false discovery rate; GC, gastric cancer; EMT, epithelial to mesenchymal transition; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GSEA, gene set enrichment analysis; NES, normalized enrichment score.