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. 2019 Dec 12;19:335. doi: 10.1186/s12935-019-1020-x

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© The Author(s) 2019

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. 2 — Knock-down of hnRNPK inhibits GC cell proliferation, migration and invasion. a The hnRNPK protein levels were detected in MGC-803 cells after treated by siRNA control or siRNA to hnRNPK (si_hnRNPK) by immunoblotting. b Cell proliferation assay of MGC-803 cells after transfected with si_control or si_hnRNPK using CCK-8. c Wound healing assays of MGC-803 cells after transfected with si_control or si_hnRNPK. The relative ratio of wound closure per field was shown in the right. d Transwell analysis of MGC-803 cells after transfected with si_control or si_hnRNPK. The relative ratio of invasive cells per field is shown below. The data are presented as the mean ± SEM, and the error bars represent the standard deviation obtained from three independent experiments. *p < 0.05