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. 2020 Jun 10;20:225. doi: 10.1186/s12935-020-01288-7

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 3 — ARHGAP30 overexpression suppressed pancreatic cancer cell proliferation, migration, and invasion and promoted apoptosis. ARHGAP30 was overexpressed in ASPC1 cells. a Cell proliferation at 0, 12, 24 and 48 h was evaluated using the CCK-8 assay. b, c Cell migration and invasion were measured using a transwell assay at 72 h. d Cell apoptosis was assessed using flow cytometry at 48 h. e The levels of the related proteins β-catenin, Bcl-2, Bax, cleaved caspase-3, MMP2, and MMP9 were analyzed using western blotting. f The mRNA expression of β-catenin, Bcl-2 and MMP2 was detected. *p < 0.05, **p < 0.01, ***p < 0.001 vs. vector