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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. 3 — Effects of NPTXR knockout on the carcinogenic and drug resistance phenotypes of GC cell lines. a-c Wound-healing migration assay a, Matrigel invasion assay b, and extracellular matrix protein adhesion assay c of parental, NPTXR-KO-1, and NPTXR-KO-2 MKN1 cells. d Flow cytometric assay of ALDH-positive control (left panels) and NPTXR-KO (test, right panels) MKN1 cells. e CCK-8 proliferation assay of 5-fluorouracil (FU) sensitivity of parental and NPTXR-KO MKN1 cells after 3 days incubation. f Growth of parental and NPTXR-KO MKN1 xenografts in BALB/c nu/nu mice. *P < 0.05. Mean ± standard deviation