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. 2020 Aug 24;9(8):75. doi: 10.1038/s41389-020-00260-4

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© The Author(s) 2020

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. 5 — a NRIP3-overexpressing and NRIP3-KD cells were treated with cisplatin, and cell viability was determined by cell growth assay. b Clonogenic survival analysis of 30-NRIP3 and 109-KD and the respective control cells (n = 3, *P < 0.05; **P < 0.01). c Representative images of cell colony formation after a radiation dose of 5 Gy for 30-NRIP3 and control cells, and 4 Gy for 109-KD and control cells. d Representative IHC images of NRIP3 in ESCC tumor tissues and paired nontumor tissues of patients receiving chemoradiotherapy (original magnification: ×200). e Overall survival analysis of the NRIP3 upregulation signature (SI_T > SI_N) in ESCC patients receiving cisplatin-based chemotherapy and/or radiotherapy (Kaplan–Meier analysis). f Overall survival analysis of the NRIP3 upregulation signature (SI_T > 4) in patients with ESCC receiving CRT or not (Kaplan–Meier analysis) (top, without CRT; bottom, with CRT) (hazard ratio was calculated using log-rank test). g Schematic model of the functional role of the NRIP3-PPARα-DDI1-RTF2 axis in conferring resistance to replicative stress in ESCC.