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. Author manuscript; available in PMC: 2022 Sep 17.
Published in final edited form as: Biochem J. 2021 Sep 17;478(17):3373–3393. doi: 10.1042/BCJ20210084

Figure 4. Control of cancer metastasis by histone modifiers.

Figure 4.

(A) EZH2 promotes cancer metastasis in prostate cancer by silencing DAB2IP with the addition of H3K27me3 on the nucleosome. (B) Loss of PRC2 complex de-represses its target CXCR4, thereby promotes metastasis in ccRCC. (C) LSD1 suppresses breast cancer metastasis by removing H3K4 methylation to silence TGFβ1. (D) KDM4A promotes head and neck SCC metastasis by activating the expression of JUN and FOSL1 through removing the H3K9me3 mark. The activation of JUN further enhanced its transcription through binding to its promoter AP-1 site. (E) KDM4C promotes breast cancer metastasis by removing H3K9me3 thereby activating the transcription of HIF1 target genes. The activation of HIF1 further enhanced its transcription through binding to the HIF-response element. (F) In breast cancer, the expression of KDM5A correlates with metastasis progression, and KDM5A activates its target TNC in a demethylase-independent manner. (G) The H4R3me2S modification can be read by PHF1, which recruits writer proteins PRMT5 and Cul4B-ubiquitin E3 ligase complex to silence its target E-cadherin and FBXW7, thereby suppresses metastasis. (H) ZMYD3 recruits KDM5D and recognizes the dual histone mark H3K14ac and H3K4me1. KDM5D then erases the methylation from histone to suppress metastasis-linked genes and metastasis progression.