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. 2020 Sep 21;12:142. doi: 10.1186/s13148-020-00937-y

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© The Author(s) 2020

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. 1 — scRNA-seq of DAC-treated HCT116 cells. a Experimental protocol of DAC treatment. HCT116 cells were seeded on day 0 and treated with 0.5 μM of DAC on days 1 and 3. The cells were placed in fresh medium without DAC on day 5, and harvested on day 7. b UMAP using 14,099 genes that can be induced by DAC treatment. DAC-treated HCT116 cells had diverse expression profiles at the single-cell level. Blue dots, mock-treated cells. Red dots, DAC-treated cells. c Unsupervised hierarchical clustering analysis using the top 200 highly upregulated genes. Genes with higher expression levels were different, depending upon DAC-treated clones. White, mock-treated cells. Red, DAC-treated cells. d, e, and f Upregulation of specific tumor-suppressor genes, ERVs, and interferon-stimulated genes. Tumor-suppressor gene methylation silenced in colorectal cancers (CHFR, FBLN2, ICAM4, and SFRP1), ERVs (ERVMER61-1 and ERVW-1), and interferon-stimulated genes (IFI16 and IFI44) were upregulated in random fractions of cells