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. 2023 Dec 20;42:346. doi: 10.1186/s13046-023-02911-x

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© The Author(s) 2023

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 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 — Knockdown of RRM2 suppressed cell growth and decreases the migration capability of ATRT cells. A Immunoblotting analyzed RRM2 knockdown efficiency. Endogenous RRM2 expression was inhibited by two independent shRRM2 (shRRM2#1 and shRRM2#2). The parental cells (WT) and luciferase shRNA (shLuc) cells were used as controls. B, C Knockdown RRM2 attenuates cell growth (B) and colony formation abilities (C) in BT12 cell. D, E Wound healing assay (D) and transwell assay (E) shows the efficiency of RRM2 depletion in ATRT cells. For each experiment, the relative values of parental cells and knockdown cells were compared with the shLuc control. Data are presented as the mean ± SD of triplicated independent experiments, ns non-significant, *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, Student’s t test