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. 2022 Aug 8;12:13540. doi: 10.1038/s41598-022-17773-0

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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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CAPOX-RT promotes ADAR1 expression more effectively than a FOLFOXIRI regimen (A) Immunohistochemical staining of ADAR1 in CRC clinical specimens treated with FOLFOXIRI (5FU + oxaliplatin + CPT-11) or CAPOX-RT (capecitabine + oxaliplatin + radiotherapy). (B) Immunohistochemical staining intensity of ADAR1 in the nucleus of CRCs treated with FOLFOXIRI or CAPOX-RT. The level of ADAR1 staining was evaluated as follows: 1, very weak; 2, weak; 3, intermediate; 4, strong; and 5, very strong. (C) ADAR1 expression was analyzed by western blot in HT29 cells. ADAR1 was upregulated by OX-RT compared with CPT-11-RT. The housekeeping gene ꞵ-actin was used as the loading control. Wilcoxon’s signed-rank test. **p < 0.01. CRC colorectal cancer, OX oxaliplatin, RT radiotherapy.