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. 2020 Aug 26;19:131. doi: 10.1186/s12943-020-01251-0

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Expression of NPTXR in GC cell lines and effect of NPTXR knockdown, knockout, or overexpression on cell phenotypes. a qRT-PCR analysis of NPTXR, MAP 1B, MMP9, and NUDT13 mRNA in the indicated human GC cell lines. b CCK-8 proliferation assay of parental and NPTXR-knockdown (KD, siRNA-mediated) MKN1, N87, and NUGC3 cells. c-f CCK-8 proliferation assay c, wound healing migration assay d, Matrigel invasion assay, e and in vivo tumorigenicity f of parental and NPTXR-KD (shRNA-mediated) MKN1 cells. g qRT-PCR analysis and CCK-8 proliferation assay of control and NPTXR-overexpressing NUGC3 cells. *P < 0.05. Mean ± standard deviation