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. 2023 Sep 1;14(9):582. doi: 10.1038/s41419-023-06108-0

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© The Author(s) 2023

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. 9 — CCL17 and CCL22 which were secreted by TAMs activated the PI3K/AKT pathway in tumor cells via CCR4. Specifically, AKT phosphorylation inactivated IP3R, and induced calcium aggregation in the ER, which further activated ATF6 and increased GRP78 expression. Excessive GRP78 bond with MRP1 and pulled it on cytomembrane, therefore, the membrane translocation of MRP1 was the direct cause of TAMs-CM-induced 5-FU efflux and resistance.