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. 2021 Mar 5;12:1455. doi: 10.1038/s41467-021-21804-1

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© This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 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 Principal component analysis of peak accessibility in SAM-, MTA-, and mock-treated activated CD8+ T cells, as well as non-activated CD8+ T cells. Dot represented the consensus peaks of CD8+ T cells underwent indicated treatment (n = 3 in each treatment condition). b Chromatin accessibility heatmap of SAM-, MTA-, and mock-treated activated CD8+ T cells. c Number of peak changes by treatments. (FDR < 0.05). d Heatmap of accessibility intensity in 3019 loci associated with T-cell signaling pathway. e ATAC-seq coverage at CD28 and PDCD1. Peaks were highlighted in yellow. f Sequence motifs enriched in the open chromatin regions of mock-treated or SAM/MTA-treated activated CD8 T cells. g Pathway analysis of the most variable peaks associated with SAM/MTA treatment (FDR < 0.05). h SAM/MTA-induced chromatin changes correlated with T-cell transcriptome changes in clinical HCC tumors. The differentially expressed ATAC-seq peaks (FDR < 0.05, fold change >1.5) and the most differentially expressed genes in HCC tumors of TIGER-LC cohort (FDR < 0.05) were compared. After excluding tumor-specific genes, we identified 12 genes as SAM/MTA-driven T-cell genes, defined as genes showed the most variable chromatin changes in SAM/MTA-treated CD8+ T cells and, coincidentally, were significantly upregulated in salvage-dominant HCC tumors. The expressions of SAM/MTA-driven T-cell genes were examined in HCC-infiltrating T cells (GEO125449). The boxplots summarize the distribution of the mean expression of SAM/MTA-driven T-cell genes obtained from salvage-dominant tumors (n = 154 T lymphocytes from three patients) to de novo-dominant tumors (n = 21 T lymphocytes from one patient). The minimum and the maximum values are described by the extension of whiskers; the medium value is indicated by the middle line within box, and the 25th and 75th percentiles are indicated by the edges of box. Statistical significance is determined by two-sided independent t test. ATAC-sequencing data are available at the GEO repository under Study Accession GSE166213. Source data are provided as a Source Data file.