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. 2019 Sep 14;25:44. doi: 10.1186/s10020-019-0111-4

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© The Author(s) 2019

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 — PRSS1_R116C mutation promotes the malignant phenotype of PANC-1 cells. a. The transwell chamber system was applied to assess the effect of PRSS1 wild type/R116C mutant overexpression on PANC-1 cell migration (converted microscope, 200×); b. The matrigel assay was performed to evaluate the effect of PRSS1 wild type/R116C mutant overexpression on PANC-1 cell invasion; c. CCK8 assay was used to measure PANC-1 cell proliferation; d. Effect of PRSS1 wild type/R116C mutant overexpression on PANC-1 cell cycle distribution; e. Flow cytometry was employed to measure the effect of PRSS1 wild type/R116C mutant on PANC-1 cell proliferation; f. R116C mutation prominently increased ERK and VEGFR2 expression in pancreatic cancer