DNA methylation-mediated Siglec-7 regulation in natural killer cells via two 5' promoter CpG sites.

Publisher: Blackwell Scientific Publications Country of Publication: England NLM ID: 0374672 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1365-2567 (Electronic) Linking ISSN: 00192805 NLM ISO Abbreviation: Immunology Subsets: MEDLINE

Original Publication: Oxford : Blackwell Scientific Publications

Antigens, Differentiation, Myelomonocytic/*genetics ; Epigenesis, Genetic/*immunology ; Killer Cells, Natural/*immunology ; Lectins/*genetics; Antigens, Differentiation, Myelomonocytic/metabolism ; Azacitidine/pharmacology ; Butyric Acid/pharmacology ; Cell Line ; CpG Islands/genetics ; DNA Methylation/drug effects ; DNA Methylation/immunology ; Epigenesis, Genetic/drug effects ; Histone Code/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/metabolism ; Humans ; Killer Cells, Natural/drug effects ; Killer Cells, Natural/metabolism ; Lectins/metabolism ; Promoter Regions, Genetic/genetics ; RNA-Seq ; Transcription, Genetic/drug effects ; Transcription, Genetic/immunology

First discovered on the natural killer (NK) cell, the cell surface inhibitory receptor sialic acid-binding immunoglobulin-like lectin-7 (Siglec-7) is known for regulating many important biological activities. However, the detail regulatory mechanism for Siglec-7 expression in NK cells currently remains unclear. In this study, we aimed to investigate how cell surface Siglec-7 expression is regulated and found that, in both NK cell lines and peripheral NK cells, transcription was the main regulatory step. Furthermore, when NK-92MI and peripheral NK cells were treated with DNA methyltransferase (DNMT) inhibitor, the CpG island, with 9 CpG sites, in 5' Siglec-7 promoter became noticeably hypomethylated, and Siglec-7 expression increased in both RNA transcript and surface protein. Within this CpG island, we identified both CpG 8 and CpG 9 as two key regulators responsible for Siglec-7 expression. Additionally, by using histone deacetylases (HDAC) inhibitor, butyric acid, we showed that Siglec-7 expression was also subjected to the histone modification. And a combined treatment with both 5-azacytidine and butyric acid showed an additive effect on Siglec-7 transcript expression in peripheral NK cells.
(© 2020 John Wiley & Sons Ltd.)

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Keywords: DNA methylation; Siglec-7; epigenetics; histone acetylation; natural killer cell

0 (Antigens, Differentiation, Myelomonocytic)
0 (Histone Deacetylase Inhibitors)
0 (Lectins)
0 (SIGLEC7 protein, human)
107-92-6 (Butyric Acid)
EC 3.5.1.98 (Histone Deacetylases)
M801H13NRU (Azacitidine)

Date Created: 20200207 Date Completed: 20201118 Latest Revision: 20210502

20221213

PMC7160663

10.1111/imm.13179

32027025