Open AccessTET2 is involved in DNA hydroxymethylation, cell proliferation and inflammatory response in keratinocytes
Author(s) -
Xinxin Liu,
Xin Wang,
Nian Liu,
Ke Zhu,
Song Zhang,
Xiaoru Duan,
Yongjun Huang,
Zhao-Hui Jin,
Himanshu Jaypaul,
Yan Wu,
Hong-Xiang Chen
Publication year - 2020
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2020.10989
Subject(s) - hacat , cell cycle , proinflammatory cytokine , viability assay , biology , microbiology and biotechnology , mtt assay , cell growth , gene knockdown , cancer research , cell , apoptosis , immunology , cell culture , inflammation , biochemistry , genetics
DNA methylation and hydroxymethylation are the most common epigenetic modifications associated with the cell cycle and the inflammatory response. The present study aimed to investigate the role of 5‑hydroxymethyl‑cytosine (5‑hmC) and ten‑eleven translocation‑2 (TET2) in keratinocytes. Following TET2 knockdown, dot blot analysis was performed to assess the levels of 5‑hmC in keratinocytes, using HaCaT cells. Subsequently, the viability and cell cycle of HaCaT cells were assessed by MTT, Cell Counting Kit‑8 assay and flow cytometric assays. Cyclin‑dependent kinase inhibitor 2A and proinflammatory cytokine protein and mRNA expression levels were also detected. The present results suggested that TET2 may play an important role in regulating cellular proliferation by mediating DNA hydroxymethylation in HaCaT cells. In addition, TET2 knockdown decreased the production of proinflammatory cytokines, including lipocalin 2, S100 calcium binding protein A7, matrix metallopeptidase 9, C‑X‑C motif chemokine ligand 1, interferon regulatory factor 7 and interleukin‑7 receptor. The present study suggested that TET2 regulated cell viability, apoptosis and the expression of inflammatory mediators in keratinocytes. Collectively, the results indicated that TET2 knockdown may relieve inflammatory responses in the skin.