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. 2021 Jan 13;14:14. doi: 10.1186/s13045-020-01030-w

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© The Author(s) 2021

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

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Fig. 3 — Effects of microenvironmental remodeling on PC progression under hypoxia. Hypoxia-driven ROS production activates PSCs to secrete various soluble factors, favoring the malignant phenotypes of PC. Hypoxia-stimulated TGF-α signaling induces Fbln5 expression through a PI3K/AKT-dependent mechanism in A-PSC, and Fbln5 competes with fibronectin for integrin binding and reduces ROS production. Upward arrows indicate upregulation of expression, and other arrows indicate positive modulations or release of molecules. Abbreviations: A-PSC, activated pancreatic stellate cells; Gem, gemcitabine; Q-PSC, quiescent pancreatic stellate cells