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. 2020 Aug 15;11(8):637. doi: 10.1038/s41419-020-02896-x

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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. 4 — Subcutaneous CCA tumors were established in mice by inoculation of RBE cells and received respective treatments as described in Supplementary Information. a The growth curve of RBE tumors was recorded. b RBE tumors were resected, weighed, and photographed at the end of experiments. c Two mice were killed from each group to harvest tumors 2 days after treatments and the expression of TTN-AS1 and miR-320a was examined by in situ hybridization (magnification ×200; Scale bar, 100 μm), and NRP-1 expression by immunohistochemistry (Magnification ×400; Scale bar, 50 μm). Tumors harvested at the end of experiments. d Illustrated are representative tumor sections immunostained by Abs against Ki-67 and CD31, respectively (Magnification ×400; Scale bar, 75 μm). In situ cell proliferation index (e) and tumoral microvessel density (f) were quantified. g Tumor tissue homogenates were immunoblotted for detecting the expression of key proliferation proteins. **P < 0.001 vs. controls; ^#P < 0.05 and ^##P < 0.001 vs. shRNA-TTN-AS1.