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. 2017 Jun 5;7:2807. doi: 10.1038/s41598-017-02901-y

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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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NKX6.3 suppresses the effects of H. pylori CagA on cell growth, ROS production, NF-kB signaling pathway and DNMT1 activity. (A and B) CagA induced a time-dependent increase in cell viability (A) and cell proliferation (B), but the expression of NKX6.3 inhibited the stimulatory effects of CagA on cell viability and proliferation. Results are represented as mean ± SEM from three independent experiments. (C) NKX6.3 abrogated CagA-induced ROS production in NKX6.3 stable cells. (D) CagA increased the expression of NF-kB p65, p50 and DNMT1 proteins and induced loss of Hace1 expression, but NKX6.3 markedly inhibited the CagA effects on expression of these proteins. (E) CagA enhanced DNMT1 activity in AGS and MKN1 cells, but NKX6.3 suppressed the CagA-induced DNMT1 activity. Results are represented as mean ± SEM from three independent experiments. (F) NKX6.3 inhibited CagA-induced hypermethylation of Hace1 gene. Each dot plot represents the result from the individual experiment. **P < 0.005, *P < 0.05, based on the student’s t-test.