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. 2022 Jun 23;79(7):377. doi: 10.1007/s00018-022-04364-5

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© The Author(s) 2022

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/.

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Fig. 1 — Development and genetic analysis of a highly brain-metastatic melanoma cell line model. A General workflow for the generation and enrichment of highly metastatic melanoma cell line clonal variants 2A and 2B from parental cell line YUGEN8. B Highly pigmented brain sample isolated from mice injected with Cl.2A tumor cells later confirmed by H&E staining. C Kaplan–Meier survival of nude mice following left ventricle injection of Cl.2A, Cl.2B, and Cl.1A cells (p < 0.0013, n = 31). D Tumor growth rates of Cl.1A, Cl.2A, and Cl.2B cells were implanted subcutaneously in athymic nude mice and monitored for 5 weeks (p > 0.05 and n = 18 for the three groups). Tumor growth was measured at study endpoint and tumor volumes shown were calculated using the ellipsoid volume formula. Scatter plots showing the correlation between the gene expression profiles of Cl.2A vs Cl.2B (E), Cl.1A vs Cl.2A (F), and Cl.1A vs Cl.2B (G), respectively. Fold changes of genes that encode for different ECM proteins overexpressed in both Cl.2A and Cl.2B vs parental YUGEN8 (H) and the metastatic indolent Cl.1A (I), respectively