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. 2018 Oct 18;9(11):1065. doi: 10.1038/s41419-018-1104-x

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© The Author(s) 2018

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. 5 — a Wound-healing assay shows the abilities of SW1990 and PANC-1 cells with SATB-1 silenced or co-cultured. b The transwell assay shows the fractions of migrated and invaded SW1990 and PANC-1 cells with SATB-1 silenced or co-cultured. Knockdown of SATB-1 inhibited the migration and invasion abilities of PANC-1 and SW1990 cells. Coculturing with CAFs enhanced the migration and invasion abilities of PANC-1 and SW1990 cells, but neutralization with anti-SDF-1 antibody reduced these abilities. Compared with control pancreatic cancer cells, n = 3, ^*p < 0.05, ^**p < 0.01, ^***p < 0.001. c Wound-healing and transwell assays show the upregulated migration and invasion abilities of Capan-2 and BXPC-3 cells transfected with pcDNA3.1-SATB-1. Compared with control pancreatic cancer cells, n = 3, ^**p < 0.01, ^***p < 0.001