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. 2021 Feb 10;21:100. doi: 10.1186/s12935-021-01803-4

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© The Author(s) 2021

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Representative image of ROS assay and colony formation capacity CSCs after being-treated with SR9243 (a). DCFH-DA assay showed an increase of fluorescence intensity in CSCs after exposure to 60 nM SR9243, indicating increased ROS content after LXR inhibition. The number of colony formation was calculated in in 3D soft agar after LXR inhibition. Data showed a statistically significant level between the control and treatment groups. Measuring the percent of apoptotic CSCs after-being treated with SR9243 and T0901317 (b). CSCs were incubated with LXR agonist (5 µM T0901317) and antagonists (60 nM SR9243) for 48 h. Student t-test and One-Way ANOVA with Tukey posthoc analysis. *p < 0.05, **p < 0.01, and ***p < 0.001