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. 2017 Dec 22;15(3):2333–2342. doi: 10.3892/etm.2017.5673

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Copyright: © Deng 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. — Sirt7 regulated CRC proliferation and invasion in an E-cadherin-dependent manner. Endogenous E-cadherin level was measured in SW620 and HCT116 cells after transduction with (A) E-cadherin siRNAs or SCR and (B) E-cadherin overexpression lentivirus or lentiviral vector GV208 (control). GAPDH served as an internal control. (C) MTT assay was performed in SW620 and HCT116 cells transfected with si-Sirt7, SCR, si-Sirt7+SCR or si-Sirt7+si-E-cadherin. The OD value was measured every 24 h. (D) Transwell assay was performed in HT29 and SW480 cells transfected with Sirt7, vector, Sirt7+vector or Sirt7+E-cadherin. Cells invading the lower chamber were stained and counted under a light microscopy, and the results were presented as the fold change over the vector. *P<0.05 and **P<0.01, vs. corresponding control group. Sirt7, sirtuin 7; CRC, colorectal carcinoma; SCR, scramble control RNA; si, siRNA.