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. 2019 Mar 20;9:4925. doi: 10.1038/s41598-019-41346-3

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© The Author(s) 2019

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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PDGF induced dephosphorylation of CAP1 in pancreatic cancer cells. (A) Treatment of serum-starved AsPC-1 cancer cells with PDGF induced CAP1 dephosphorylation at S308/S310. Cells were cultured overnight, serum-starved for 24 hrs, followed by treatment with 30 ng/ml PDGF for indicated time durations. Cell lysates were prepared and used in the Western blotting with a phosphor-specific antibody that detects phosphor signals on both residues of the tandem regulatory site on CAP1. The dephosphorylation effect was most significant at the 5-minute time point of PDGF treatment. (B) Treatment of serum-starved PANC-1 cells with PDGF also induced remarkable CAP1 dephosphorylation, in similar fashion with AsPC-1 cells. Treatment of cells and Western blotting were conducted following the same procedures as used for AsPC-1 cells. GAPDH served as a loading control in Western blot.