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. 2020 Jun 3;39:102. doi: 10.1186/s13046-020-01602-1

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© The Author(s) 2020

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Verteporfin treatment inhibited tumor development in E6-E7 knock-in mice with 4NQO-induced OSCC. a Schema of 4NQO-induced OSCC transgenic mice model that were treated with VP (100 mg/kg) at a 3-day interval for 6 doses. b, c Representative images of tongue lesions, lesions size and number in Vehicle-treated or VP-treated mice (n = 8 per group). d Representative images of H&E staining from tumors of Vehicle-treated or VP-treated mice. Scale bars, 50 μm. e Expressions of CCL2 and CD163 by qRT-PCR in tumors of Vehicle-treated or VP-treated mice. Quantitative analysis based on triplicate experiments. Results were presented as means ± SD. *P<0.05, **P<0.01, ***P<0.001