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. 2019 Feb 20;9:2399. doi: 10.1038/s41598-019-38643-2

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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/.

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Role of host-dependent CXCR4 signaling in experimental metastasis formation in the zebrafish xenograft model. Inoculation of human tumor cells into the blood circulation of zebrafish embryos results in experimental metastasis formation, characterized by tumor cell aggregates in the blood vessels, and extravasation and invasion in the surrounding tissue, in the region of the caudal hematopoietic tissue (CHT). During early metastatic events, endothelium alteration takes place and neutrophils localize in the surrounding of the tumor cells. The CHT is a vascular plexus in the tail fin between the DA and the CV and is a hematopoietic site. Upon disruption of the host CXCR4 (Cxcr4b) signaling, cancer cells are unable to initiate early metastatic events. Neutrophils are preferentially retained in the CHT and fail to accumulate at tumor metastatic sites.