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. 2022 Apr 11;41:136. doi: 10.1186/s13046-022-02346-w

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© The Author(s) 2022

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. 4 — YBX1 promotes lung cancer cell proliferation and migration. A CCK-8 (at 24, 48, 72 and 96 h after transfection) and (B) EdU assays (at 48 h after transfection) were performed to assess the effect of YBX1 knockdown and over-expressing on A549 cell proliferation. C Flow cytometry using Annexin V-FITC/PI staining was performed to analysis apoptosis of YBX1 knockdown and overexpressing A549 cells (at 24 h after transfection). D Colony formation assay with A549 cells at 7 d after knockdown and overexpression of YBX1.The effect of YBX1 knockdown and overexpression on A549 (E) migration and (F) invasion was examined by transwell assay (at 24 h after transfection). Data from three independent experiments are shown as the mean ± SD (error bars). *P < 0.05, **P < 0.01, ***P < 0.001 (Student’s t-test). NC: negative control