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. 2018 Jul 25;37:169. doi: 10.1186/s13046-018-0846-8

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 3 — TPT1-AS1 promotes tumor growth and metastasis in vivo. a Tumor growth curve revealed that TPT1-AS1 overexpression significantly promoted, while TPT1-AS1 knockdown inhibited tumor growth in vivo (n = 5). b Representative HE staining of lung metastases in TPT1-AS1 overexpression or knockdown cells (n = 5). c Tumor nodules were subjected to immunohistochemical staining for Ki-67 assays and quantitative analysis. Representative immunostaining assays revealed that TPT1-AS1 overexpression significantly increased the number of Ki-67 positive cells. However, the percentage of Ki-67 positive cells in tumors arising from the TPT1-AS1 knockdown group was significantly lower than that in the negative control group. d Immunohistochemistry of E-cadherin and Vimentin were showed and compared between tissues of respective TPT1-AS1 expression level. e Immunohistochemistry of E-cadherin and Vimentin were showed and compared between TPT1-AS1 high expressing CC tissues (n = 59) and TPT1-AS1 low expressing cases (n = 56). *P < 0.05