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. 2019 May 24;121(1):65–75. doi: 10.1038/s41416-019-0483-9

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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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Fig. 2 — S100A14 sustains epithelial morphology and suppresses cell invasion. a Subcellular localisation of S100A14 was examined in BxPC-3 and SU.86.86 epithelial PDAC cell lines, and in human pancreatic duct epithelial (HPDE) cells by immunofluorescence. Nuclei are stained in blue (DAPI). b Phase-contrast images of PDAC epithelial cells transfected with S100A14-targeting or control siRNAs. S100A14 knockdown results in cell scattering. c Depletion of S100A14 stimulates invasion of epithelial PDAC cells in zebrafish embryos. Bars represent means (n = 3 biological replicates; 10 fish in each experiment)+/− StDev. *p < 0.05; **p < 0.01 (Student’s t-Test). Western blots illustrate the degree of S100A14 depletion. Knockdown of S100A14 enhances expression levels of mesenchymal S100 proteins, but not canonical EMT markers, E-cadherin and vimentin (data not shown)