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. 2021 Feb 26;7:38. doi: 10.1038/s41420-021-00421-3

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© The Author(s) 2021

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. 6 — A SW480 cells were implanted subcutaneously in nude mice, and randomly divided into 4 groups (N = 6). Each group was intraperitoneal injection with control solvent (normal saline, PEG300, and DMSO), avasimibe (15 mg/kg.d), nystatin (4 mg/kg.d) and combined drugs. After 4 weeks, the xenografts were measured and weighed. The bar graphs indicate tumor volume and weight of each group. B Representative pictures of YAP staining in xenograft tumor tissues. The graph indicates the IHC scores of YAP expression. Scale bar: 20 μm. C Mouse models of AOM/DSS-induced colorectal cancer were described in ‘Materials and methods’ section. The mice were randomly divided into 4 groups (N = 5), each group was intraperitoneally injected with control solvent, avasimibe (15 mg/kg.d), nystatin (4 mg/kg.d) and combined drugs during the period of drinking normal water. The graphs showed the average number and tumor area of each group. Statistical methods: one-way ANOVA followed by Tukey post hoc test, *p < 0.05, **p < 0.01, ***p < 0.001, NS indicates no significant difference. D The model of regulation of YAP by cholesterol in colon cancer. LRP6 is released from the cholesterol-rich membranes (lipid rafts) and directly binds to FZD7, resulting in the inactivation of PCP-YAP pathway and classical Wnt pathway when lack of cholesterol. After membrane cholesterol levels increased, LRP6 is transfered to cholesterol-rich area, alleviating the inhibitory effect of LRP6 on PCP-YAP pathway, and activating classical Wnt pathway simultaneously.