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. 2020 Mar 9;11:1270. doi: 10.1038/s41467-020-15003-7

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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. 1 — a RNF113A expression in lung cancer. Western blot (WB) analyses with human lung tumors (“T”) and corresponding normal adjacent tissues (“N”). Numbers refer to the percentage of tumor cells. b. Subcellular localizations of RNF113A in lung adenocarcinomas. Anti-RNF113A Immunohistochemistry analyses were conducted on a Tissue-MicroArray (TMA) (×40 objective). Stromal cells served as internal negative control. c Patients with high levels of RNF113A mRNAs show a shorter survival rate (Kaplan-Meir plot). d, e RNF113A expression is induced by Cisplatin in A549 (d) or BZR-T33 (e) cells. On the top, RNF113A mRNA levels in unstimulated cells is set to 100% and levels in other experimental conditions are relative to that after normalization with β-actin. Data from two independent experiments performed in triplicates (means ± SD) are shown. At the bottom, WB analyses. The anti-pDNA-PKcs (S2056) antibody was used to prove DNA damage. f Induction of RNF113A expression by Cisplatin in A549 cells (immunofluorescence analyses). g, h RNF113A expression is induced by Camptothecin in A549 (g) or BZR-T33 (h) cells. On the top, data from two Real-time PCR (independent) analyses performed in triplicates (means ± SD) are plotted as described in (d). At the bottom, WB analyses. i RNF113A induction by Cisplatin occurs through a C/EBPβ-dependent pathway. Control or C/EBPβ-depleted A549 cells were treated or not with Cisplatin (25 μM) for 24 h and WB analyses were done. Expo. = exposure. j C/EBPβ is recruited on the RNF113A promoter. C/EBPβ binding sites were identified (Tfbind software) and ChIP assays using an anti-C/EBPβ antibody were carried out. Histogram show recruitment C/EBPβ on indicated sites with or without treatment (IgG antibody was used as negative control). RNF113A promoter is lacking a TATA box. Results of two independent experiments (means ± SD, Student t-test, ***p < 0.001, **p < 0.01, *p < 0.05) are shown. START = start of transcription. k RNF113A expression is not regulated by p53. A549 cells were incubated or not with JNJ-2685416 or with Nutlin and WB analyses were done. Source data for all figures are provided as a Source Data file.