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. 2016 Aug 31;16(1):701. doi: 10.1186/s12885-016-2730-2

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© The Author(s). 2016

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. 4 — Reactive oxygen species mediate pristimerin inhibited SPHK-1 activity in hypoxic PC-3 cells. Hypoxic PC-3 cells were treated with pristimerin and/or NAC. a Western blotting was performed to determine the expression of SPHK-1, HIF-1α, p-AKT, AKT, pGSK-3β, GSK-3β, and β-actin in hypoxic PC-3 cells. b SPHK-1 activity in pristimerin and/or NAC-treated PC-3 cells under hypoxia. Data are presented as means ± SD. * p <0.05 and ** p <0.01 compared with hypoxia control. # p <0.05 compared with normoxia control. c Pristimerin suppresses p-AKT and p-GSK-3β via SPHK-1 inhibition in prostate cancer cell lines under hypoxia. Western blotting was performed to determine the expression of SPHK-1, HIF-1α, p-AKT, AKT, pGSK-3β, GSK-3β, and β-actin in hypoxic PC-3 cells