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Epigallocatechin‐3‐gallate inhibits proliferation and induces apoptosis in odontogenic keratocyst keratinocytes
Author(s) -
Yang Shao-Bin,
Pang Bao-Xing,
Xue Jiao,
Yuan Rong-Tao
Publication year - 2019
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.13073
Subject(s) - apoptosis , keratinocyte , keratocyst , cell growth , cell cycle , cytokeratin , flow cytometry , cancer research , biology , chemistry , in vitro , microbiology and biotechnology , immunohistochemistry , pathology , medicine , immunology , odontogenic , biochemistry
Abstract Objective The aim of this study was to investigate the effects of epigallocatechin‐3‐gallate on the proliferation and apoptosis of odontogenic keratocyst (OKC) keratinocytes in vitro. Materials and methods Keratinocytes isolated from the epithelial lining of the OKC were cultured in keratinocyte serum‐free medium and identified by CK10, CK14, pan‐cytokeratin and vimentin immunofluorescence staining. The cells were exposed to EGCG at different concentrations, and proliferation inhibition was measured by cell counting kit 8 assay. Cell cycle and apoptosis were assessed by flow cytometry, and expression of the WNT signalling pathway‐related proteins FZD3 and JNK3 was detected by quantitative real‐time PCR and Western blotting. Human oral keratinocytes (HOKs) were used as the control. Results The OKC keratinocytes were successfully cultured. The primary cells were tile‐like and expressed the epithelial biomarkers CK10, CK14 and pan‐cytokeratin. Epigallocatechin‐3‐gallate inhibited cell proliferation in a dose‐ and time‐dependent manner, arrested cell cycle in the G 1 phase and induced apoptosis of OKC keratinocytes. FZD3 and JNK3 were overexpressed in OKC keratinocytes compared with HOKs and were downregulated by epigallocatechin‐3‐gallate treatment. Conclusion Epigallocatechin‐3‐gallate inhibited proliferation and induced apoptosis in OKC keratinocytes, possibly by suppressing the WNT/JNK signalling pathway. It may thus be potentially used for OKC treatment.