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. 2021 Nov 13;7:354. doi: 10.1038/s41420-021-00743-2

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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, B Following exposure to NCT-58, CD44 and ALDH1 expression levels were markedly downregulated in JIMT-1 xenograft tumors. The fluorescence intensities of CD44 (A, ***p < 0.001, n = 6) and ALDH1 (B, ***p < 0.001, n = 6) were analyzed using a histogram tool. C–E Effect of NCT-58 on induction of the HSR in vivo. C NCT-58 administration resulted in a decrease in nuclear expression of HSF-1 (green). Fluorescence intensity of HSF-1 localized in the nuclei is represented in arbitrary units as defined by the software using the intensity profile tool. D, E NCT-58 downregulated both HSP70 and HSP90 expression. Quantitative graphs of fluorescence intensities of HSP70 (D, **p < 0.01, n = 6) and HSP90 (E, ***p < 0.001, n = 6) signal, shown in the bottom panels, respectively. Tumors were harvested within 24 h of the last administration of NCT-58 for immunohistochemistry assessment. Data were analyzed by unpaired Student’s t-test.