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Fig. 1 | Journal of Biomedical Science

Fig. 1

From: Epigenetic remodeling of the immune landscape in cancer: therapeutic hurdles and opportunities

Fig. 1

Epigenetic regulation of innate immune cells in the tumor immune microenvironment. In natural killer (NK) cells, histone methyltransferases (ASH1L and JARID2) and histone demethylases (KDM6B and UTY) promote NK activation via upregulating activation-related gene expressions. By contrast, EZH2 and DNMTs suppress the expression of activating NK receptors, such as NKG2D. In macrophages, activation of monocyte (M0) is positively regulated by SETD4 and negatively regulated by ASH1L, SMYD2, and SMYD5, respectively. Epigenetic modifiers are also involved in the polarization process of macrophages. SETD7, SMYD3 and DNMTs promote M1 polarization, whereas EHMT2, KDM6B, PRMT1, KAT2A/B, EP300 and TET promote M2 polarization. Tumor-associated macrophages (TAMs) often exhibit an M2-like phenotype. H3K4me1: mono-methylation at the 4th lysine residue of the histone H3. H3K4me2: di-methylation of lysine 4 on histone H3. H3K27me3: tri-methylation of lysine 27 on histone H3. “Me” in red circle: methyl group. “Ac” in purple circle: acetyl group. AcH3: histone H3 acetylation. KIRs: killer Ig-like receptors. PRF: perforin. GzmB: granzyme B. This figure was created on BioRender.com

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