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. 2016 Feb 29;9:10. doi: 10.1186/s13048-015-0210-y

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© Chen et al. 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. 2 — Knockdown of WFDC2 expression reduces cell proliferation and enables an E2 response in SK-OV-3 ovarian cancer cells. HO8910 (a) or SKOV-3 (b) cells were treated with or without E2 (625 ng/ml) and knockdown of WFDC2 reduced the viable cell number compared with the negative control. n = 3 *P < 0.05; **P < 0.01. E2 response of HO8910 (c) and SKOV3 (d) cells. Knockdown of WFDC2 enabled an E2 response in SK-OV-3 ovarian cancer cells. HO8910 (e) or SKOV-3 (f) cells were treated with E2 (625 ng/ml) alone or in combination with TAM (100 ng/ml), and knockdown of WFDC2 increased the inhibition efficiency in ovarian cancer cells by adding TAM compared with the control; *P < 0.05, **P < 0.01 for TAM versus the control. ∆P < 0.05, verus cells treated with TAM without ShRNA interference