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. 2021 Jun 28;28(12):3357–3370. doi: 10.1038/s41418-021-00823-x

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© The Author(s) 2021

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — HCT116 wild-type (WT) and mutant cells were tested for mRNA expression of the MKI67 and the CDK inhibitor CDKN1A/p21 genes. Clonal cell lines for WT (n = 4), RB^−/− (n = 3), LIN37^−/− (n = 4), or double-knockout LIN37^−/−; RB^−/− (n = 2) cells were treated with nutlin-3a or doxorubicin for 48 h. As controls, untreated or DMSO (solvent control)-treated (48 h) cell lines were analyzed. Levels of mRNA from CDKN1A/p21 and MKI67 genes were determined by real-time RT-qPCR. The log2-fold changes in mRNA expression of treated vs. control cells are given. Mean values are indicated by black bars. Significances were calculated using the Student’s t-test (n.s., not significant; *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001).