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. 2017 May 22;7:2229. doi: 10.1038/s41598-017-02494-6

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© The Author(s) 2017

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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HMGA2 is associated with the EMT signaling. MKN74 and MKN28 cells stably transfected with HMGA2 expression plasmid and MGC803 and MKN45 cells stably transfected with HMGA2 sh-RNA plasmid. (A) Immunofluorescence staining. Overexpression of HMGA2 increased the protein expression of vimentin and inactivated the expression of E-cadherin and HMGA2 silencing inhibited vimentin expression and upregulated E-cadherin expression (bar, 50 um). (B) Western blot showed that expression of E-cadherin and vimentin, N-cadherin in GC cell lines (*P < 0.05). (C) IHC staining showed the expression of E-cadherin and vimentin in GC samples (×200, bar 50 um). (D,E) Kaplan-Meier survival analysis of GC patients categorized by a combination of HMGA2 and E-cadherin (D), vimentin (E) (*P < 0.05).