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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. 5 — Activated RHOA contributes to the regulation of ARHGAP30/β-catenin in pancreatic cancer. a RHOA activity was detected in ARHGAP30-overexpressing ASPC1 cells using western blotting. b RHOA activity was detected in ARHGAP30-silenced SW1990 cells using western blotting. c β-Catenin was detected using western blotting in cells subjected to ARHGAP30 knockdown and CCG-1423 (RHOA inhibitor) treatment. **p < 0.01, ***p < 0.001 vs. vector or shNC; ^###p < 0.001 vs. shARHGAP30