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. 2018 Aug 16;18:824. doi: 10.1186/s12885-018-4717-7

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© The Author(s). 2018

Open Access This 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 — CCKBR mediated suppressive effects of gastrin on ER⁺ BC cells. a ER⁺ MCF-7, as well as T-47D and ER⁻ MDA-MB-231 BC cells were treated with gastrin (10^− 7 M) for 7 d. CCK-8 assay results demonstrated that gastrin inhibited proliferation of MCF-7 (a) and T-47D (b), but not MDA-MB-231 (c) cells. (b-c) Knockdown of CCKBR by CCKBR-targeted siRNA blocked the effects of gastrin on ER⁺ BC cells. (a) Expression of CCKBR in MCF-7 and T-47D cells transfected with CCKBR-targeted siRNA for 48 h. (b) Gray density analysis demonstrated about two-thirds of CCKBR were downregulated in MCF-7 and T-47D cells (*P < 0.01). (c) CCK-8 assay results demonstrated that knockdown of CCKBR blocked the inhibitory effects of gastrin on MCF-7 and T-47D cells (*P < 0.05). d MCF-7 BC tumors grew much slower in animals treated with gastrin. (a) Growth curves of MCF-7 tumors in control and experimental mice (*P < 0.01). (b) The panel shows tumors removed from mice 12-d post-gastrin treatment (control, N = 6; gastrin treatment, N = 6). (c) Weight of tumors removed from mice 12-d post-gastrin treatment (control, N = 6; gastrin treatment, N = 6; *P < 0.05)