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. 2018 Aug 10;8:11955. doi: 10.1038/s41598-018-29878-6

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Silencing AEBP1 results in the inhibition of epithelial-mesenchymal transition (EMT) by downregulating the NF-κB pathway. (A) qRT-PCR and (B) Western blotting analyses of EMT-related markers (E-cadherin, MMP2, MMP9, snail and vimentin) in AEBP1-knockdown and mock cells; *P < 0.05; **P < 0.01, ***P < 0.001. (C) Protein levels of p65, p-p65, IκBα and p-ERK1/2 in AEBP1-knockdown and mock cells. (D) Nuclear protein expression of NF-κB p65 in AEBP1-knockdown and mock cells. (E) Western blotting analyses of p65 and p-p65 expression in xenograft tumors derived from the AEBP1-knockdown and mock MGC803 and XN0422 cells. (F) Protein levels of two NF-κB downstream targets (CXCR4 and ICAM1) in AEBP1-knockdown and mock cells. The western blots were derived under the same experimental conditions from the same cell lysates; the original full-length Western blot images are shown in Supplementary Fig. S5.