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. 2017 Aug 29;7:9711. doi: 10.1038/s41598-017-09859-x

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© The Author(s) 2017

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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p53-dependent repression of DPYD is dependent on signaling from ATM and DNA-PK following TS inhibition. (A) Rescue of DPYD repression by inhibition of DNA damage response, HCT-116-WT and p53 ^−/− cells treated with 5-FU, with ATM (KU-55933) and DNA-PK (NU7026) inhibitors for 24 hrs. (B,C) Co-treatment with ATM and DNA-PK inhibitors relieves inhibited DPYD expression following targeting of TS with siRNA (TSsi) and Tomudex. The effects of siRNA targeting of DPYD on 72-hr cell-viability of HCT-116-WT and p53 ^−/− cells following treatment with isotoxic doses of 5-FU (D) and Tomudex. (E) High expression of DPYD mRNA predicts poor disease-free survival in colorectal cancer patients mainly with Duke Stage B and C as analyzed from the GSE14333 (Melbourne) data set. P-value was calculated by cox regression analysis (Cox P-Value = 0.00105).