TET1 exerts its anti-tumor functions via demethylating DACT2 and SFRP2 to antagonize Wnt/β-catenin signaling pathway in nasopharyngeal carcinoma cells.

Tytuł:: TET1 exerts its anti-tumor functions via demethylating DACT2 and SFRP2 to antagonize Wnt/β-catenin signaling pathway in nasopharyngeal carcinoma cells.
Autorzy:: Fan J; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Zhang Y; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Mu J; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
He X; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Shao B; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Zhou D; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Peng W; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Tang J; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jiang Y; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ren G; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xiang T; Chongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China. .
Źródło:: Clinical epigenetics [Clin Epigenetics] 2018 Aug 03; Vol. 10 (1), pp. 103. Date of Electronic Publication: 2018 Aug 03.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: Oct./Nov. 2011- : London : BiomedCentral
Original Publication: Berlin : Springer-Verlag
MeSH Terms:: Wnt Signaling Pathway*
Carrier Proteins/*genetics
Membrane Proteins/*genetics
Mixed Function Oxygenases/*genetics
Nasopharyngeal Carcinoma/*genetics
Nasopharyngeal Neoplasms/*genetics
Neoplasm Proteins/*genetics
Proto-Oncogene Proteins/*genetics
Adaptor Proteins, Signal Transducing ; Aged ; Apoptosis ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; DNA Methylation ; Down-Regulation ; Epigenesis, Genetic ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Middle Aged ; Promoter Regions, Genetic ; Sequence Analysis, DNA
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Grant Information:: #81572769;81372238 International National Natural Science Foundation of China; 2016ZDXM006 International Natural Science Foundation of Chongqing
Contributed Indexing:: Keywords: Demethylation; Nasopharyngeal carcinoma; TET1; Tumor suppressor; Wnt pathway
Substance Nomenclature:: 0 (Adaptor Proteins, Signal Transducing)
0 (Carrier Proteins)
0 (DACT2 protein, human)
0 (Membrane Proteins)
0 (Neoplasm Proteins)
0 (Proto-Oncogene Proteins)
0 (SFRP2 protein, human)
EC 1.- (Mixed Function Oxygenases)
EC 1.- (TET1 protein, human)
Entry Date(s):: Date Created: 20180805 Date Completed: 20190715 Latest Revision: 20230928
Update Code:: 20240104
PubMed Central ID:: PMC6091063
DOI:: 10.1186/s13148-018-0535-7
PMID:: 30075814
: Czasopismo naukowe

Pełny tekst

Background: TET1 is a tumor suppressor gene (TSG) that codes for ten-eleven translocation methyl cytosine dioxygenase1 (TET1) catalyzing the conversion of 5-methylcytosine to 5-hydroxy methyl cytosine as a first step of TSG demethylation. Its hypermethylation has been associated with cancer pathogenesis. However, whether TET1 plays any role in nasopharyngeal carcinoma (NPC) remains unclear. This study investigated the expression and methylation of TET1 in NPC and confirmed its role and mechanism as a TSG.
Results: TET1 expression was downregulated in NPC tissues compared with nasal septum deviation tissues. Demethylation of TET1 in HONE1 and HNE1 cells restored its expression with downregulated methylation, implying that TET1 was silenced by promoter hypermethylation. Ectopic expression of TET1 suppressed the growth of NPC cells, induced apoptosis, arrested cell division in G0/G1 phase, and inhibited cell migration and invasion, confirming TET1 TSG activity. TET1 decreased the expression of nuclear β-catenin and downstream target genes. Furthermore, TET1 could cause Wnt antagonists (DACT2, SFRP2) promoter demethylation and restore its expression in NPC cells.
Conclusions: Collectively, we conclude that TET1 exerts its anti-tumor functions in NPC cells by suppressing Wnt/β-catenin signaling via demethylation of Wnt antagonists (DACT2 and SFRP2).

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