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. 2020 Aug 26;39(40):6327–6339. doi: 10.1038/s41388-020-01431-8

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© The Author(s), under exclusive licence to Springer Nature Limited 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. 4 — a Schematic representation of DMBA-TPA chemical induced carcinogenesis in cK5-rtTA mice and cK5-rtTA/Tet-E2/E4/E5 mice models. b All 10 cK5-rtTA mice did not exhibit any tumors, while 1 in 8 cK5-rtTA/Tet-E2/E4/E5 mice developed SCC at 14 weeks. Representative photos, H&E staining, Ki67 IHC, Ki67 IF pictures were shown. Lesions of cK5-rtTA and cK5-rtTA/Tet-E2/E4/E5 mice showed more pronounced Ki67 expression (brown in IHC, red in IF) on cK5-rtTA/Tet-E2/E4/E5. DAPI (blue) and cytokeratin 1 (green) were applied to contrast the tissues in IF. Insets showed single-channel for Ki67 in IF. Scale bars: 100 μm. c cK5-rtTA/Tet-E2/E4/E5 group has significant poorer prognosis compared with control group comparing the disease-free survivals (P = 0.02). P value was calculated using the Log-rank test.