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. 2019 May 14;38:194. doi: 10.1186/s13046-019-1188-x

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© The Author(s). 2019

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. 10 — AGAP2-AS1 mediates the promoting effects of hypoxia on metastasis and EMT of HCC cells. a The expressions of HIF-1α in different time points in normoxia and hypoxia condition. b The levels of AGAP2-AS1 in Hep3B cells cultured in normoxia and hypoxia. c Transwell assays revealed that hypoxia promoted migration and invasion of Hep3B cells, while AGAP2-AS1 knockdown abolished the effects of hypoxia. d Hypoxia facilitated the EMT process of Hep3B cells and AGAP2-AS1 knockdown showed an opposite effect. *P < 0.05