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. 2019 Oct 7;14:43. doi: 10.1186/s13020-019-0263-8

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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. 5 — Effects of TKSE on the malignant properties of HT-29 cells. a The expressions of HIF-1α and its downstream gene VEGF were assessed by western blotting in hypoxia-induced HT-29 cells treated with TKSE. b Production of VEGF in hypoxia-induced HT-29 cells treated with TKSE. Cells were treated with various concentrations of TKSE under hypoxia for 24 h. Results are presented as the means ± SDs of triplicate wells. Significance vs. CoCl₂-treated group, **p < 0.01, ***p < 0.001. c A wound healing migration assay was used to observe the effects of TKSE on HT-29 cell motility. d Representative images of Matrigel transwell invasion by TKSE-treated HT-29 cells. Original magnification, ×100