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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. 3 — COH29 showed an anticancer effect on ATRT cells. A IC50 values of COH29 in BT12, Re1P6 and CHLA266 cells. B, C Analysis of cell proliferation (B) and colony formation (C) in COH29-treated cells. D Wound healing assay after cells were treated with COH29 in three days. E Transwell assay analyzed the migration ability of Re1P6 cells after being treated with COH29. A relative rate of cell migration was analyzed from the number of the cells migrating per chamber compare with the control. In all experiments, 0.1% DMSO was treated as the 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