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. 2019 Jul 2;11:98. doi: 10.1186/s13148-019-0698-x

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

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Fig. 7 — RNF40 knockdown cells with restored growth capacity show decreased tumorigenic properties. The effect of RNF40 knockdown in combination with Z-VAD treatment was tested in three independent experiments. a The clonogenic potential of HCT116 siRNF40 cells was reduced compared to wild-type controls. This phenotype was not rescued after Z-VAD-mediated caspase inhibition (n = 2). Mean ± SEM, one-way ANOVA. b Migration potential was tested using a trans-well migration assay for 48 h. Z-VAD treatment increased the proportion of migrating cells under RNF40 knockdown conditions which was still significantly lower compared to wild-type cells (n = 3). Mean ± SEM, one-way ANOVA