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. 2019 Jan 30;9:978. doi: 10.1038/s41598-018-37425-6

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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/.

PMC Copyright notice

Proposed mechanism of how solid stress signal transduction via Akt pathway regulates GDF15 expression to induce pancreatic cancer cell migration. The development of solid stress during the growth of several solid tumors, such as pancreatic cancer, activates Akt pathway which in turn phosphorylates CREB1. Subsequently, the activated CREB1 acts as transcription factor by a direct binding onto the promoter region of GDF15. GDF15 is then secreted and acts in an autocrine manner to promote pancreatic cancer cell migration.