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. 2020 Apr 15;20:122. doi: 10.1186/s12935-020-01188-w

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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 — Hedgehog/SMO/GLI1 signaling plays an essential role for targeted activation of Tenascin-C (TNC) in colorectal cancer (CRC). a Immunohistochemical staining of SMO, GLI1 and TNC in CRC tissues (original magnification ×200). Scale bar represented 100 μm. b, c Immunofluorescence staining for GLI1 and TNC in the HT29 and HCT116 cell lines. Blue for DAP1; green for GLI1; red for TNC; double labeling for Merge. d, e Protein expression of GLI1 and TNC after treatment with DMSO and 20 μM GLI1 inhibitor GANT61 (GAN) in HT29 and HCT116 cells, respectively. Western blotting data were normalized to those for β-actin and expressed as fold changes relative to levels in the control group. **P < 0.01, ***P < 0.001 versus control