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. 2022 Jan 24;12:1248. doi: 10.1038/s41598-022-05193-z

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© The Author(s) 2022

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/.

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Selumetinib combined with KRT-232 induces apoptosis in vivo. (A) IHC analysis of PDX.004 CRC tumor samples obtained from the control, selumetinib, KRT-232, or combination treatment groups. (200 × magnification). Box plots of in vivo IHC H-score of p21, p53, and cleaved caspase 3 (CC3), and percentage of Ki-67–positive tumor cells. Values represent mean ± SD. Statistical significance was determined using the Student’s t-test. (B) Heatmap generated (with false discovery rate [FDR] 0.05) from RPPA samples obtained from selumetinib-only treated PDXs vs untreated controls demonstrated 10 differentially expressed proteins (DEPs), where samples were clustered by the treatment. (C) Scatter plot created from RPPA samples obtained from the control, selumetinib, KRT-232, or combination treatment groups demonstrating the relative expression of p21. Bars show mean ± SD. (D) Heatmap generated (with FDR 0.05) from RPPA samples obtained from PDXs treated with selumetinib plus KRT-232 vs untreated controls demonstrated 91 DEPs; samples were clustered by treatment.