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. 2024 Jan 6;8:6. doi: 10.1038/s41698-023-00493-7

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© This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 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 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 — Based on our in vitro human melanoma cell models and ex vivo human melanoma TMA study as well as TCGA melanoma database analysis, we identified a previously unknown PLK1 phosphorylation site on NUMB protein that might be involved in melanoma cell migration, invasion, and EMT. Additionally, our study suggested that PLK1 inhibition altered the NOTCH pathway and EMT-related molecular consequences, which may ultimately lead to improved survival of patients with melanoma. This figure was created using BioRender.