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. 2021 Aug 17;19:353. doi: 10.1186/s12967-021-03018-7

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© The Author(s) 2021

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. 7 — FGF11 knockdown inhibits NSCLC tumorigenesis in vivo. A549 and NCI-H460 cells were infected with FGF11 shRNA and FGF11 overexpression lentivirus. Cells were inoculated into balb/c nude mice (n = 5 mice/group). A The tumor growth curve in FGF11 shRNA and control group. B Tumor weight quantification in FGF11 shRNA and control group. C Immunohistochemistry (IHC) analysis of Ki-67 expression in FGF11 shRNA and control group. D The tumor growth curve in FGF11 overexpression and control group. E Tumor weight quantification in FGF11 overexpression and control group. F Immunohistochemistry (IHC) analysis of Ki-67 expression in FGF11 overexpression and control group. The results are represented as mean ± standard derivation. *P < 0.05, ** P < 0.01, ***P < 0.005 vs. control group