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. 2018 Aug 24;8:12776. doi: 10.1038/s41598-018-30692-3

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© The Author(s) 2018

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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Pictorial Abstract. A schematic summary showing how nuclosamide through the dysregulation of the Wnt/β-catenin signaling pathway, inhibits the stemness of OSCC cells via the downregulation of pluripotency transcription factors, suppress oral CSC -associated EMT and metastasis by upregulating vimentin and snail, while downregulating E-cadherin, as well as limit EMT-related extracellular matrix (ECM) remodeling by modulation of TIMP2, MMP2 and MMP9. Similarly, nuclosamide suppresses the cisplatin-induced oral CSC enrichment and enhances the sensitivity of the ALDH+ OSCC cells to cisplatin.