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. 2024 Apr 24;14:9471. doi: 10.1038/s41598-024-59845-3

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© The Author(s) 2024

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 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/.

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Working model. The data presented in this manuscript support the conclusion that in high systemic LDL conditions induced by a high cholesterol diet, breast tumor cells when exposed to high levels of LDL have increased intravasation capacity. Mechanistically, the data suggest that LDL induces the expression of SERPINE2 and the intercalation of tumor cells with endothelial cells. Tumor cell intercalation in blood vessels facilitates intravasation and increase the probability of metastasis.