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. 2019 Feb 11;38(23):4590–4604. doi: 10.1038/s41388-019-0743-4

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© The Author(s) 2019

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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Fig. 7 — IGFBP5 activates p53 signaling pathway in GC. a p53 mRNA and (b) protein was up-regulated by PKNOX2 overexpression in AGS and MKN45 cells; while an opposite trend was observed for GES1 cells. c PKNOX2 binds to the promoter of TP53. Binding motif of PKNOX2 was predicted by JASPAR database (red squares). ChIP-PCR validated the interaction between PKNOX2 and p53 promoter region. d PKNOX2 induced p53 luciferase activity in AGS and MKN45 cells(both P < 0.0001). e p53 signaling pathway PCR array showed that PKNOX2 overexpression up-regulated numerous p53 target genes in AGS and MKN45 cells. f Validation of differentially expressed genes by real-time PCR and RT-PCR. g and h Knockdown of IGFBP5 partly abolished the induction of p53 by PKNOX2 in AGS cells, as evidenced by real-time PCR and Western blot. IGFBP5 knockdown also down-regulated p53, p21 and p27 expression in GES1 cells. (*P < 0.05; **P < 0.01; ***P < 0.0001)