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. 2019 Nov 18;8(12):68. doi: 10.1038/s41389-019-0177-4

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© The Author(s) 2019

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 — CD133Hi cells had decreased GR activity as seen by dual luciferase reporter activity assay. Silencing GAS5 and Sox2 increased GR transcriptional activity (a). Further, inhibition of GAS5 decreased cell cycle genes like CDK4 and Cyclin D2 at transcriptional (b) and well as translational (c) level. Upon treatment with glucocorticoid, dexamethasone, GR transcriptional activity in CD133Hi cells was increased, indicating a rescue from GAS5 mediated inhibition (d). Proliferation of CD133Hi cells SU86.86 was also increased upon treatment with dexamethasone (e). NF-kB transcriptional activity was negatively regulated by dexamethasone in CD133Hi cells (f). Further, silencing GAS5 and Sox2 inhibited NF-kB transcriptional activity (g). Schematic figure showing how Sox2-GAS5 axis modulates “stemness” associated properties like quiescence in metastasis in CD133hi cells.