Αρχειοθήκη ιστολογίου

Αλέξανδρος Γ. Σφακιανάκης
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5
Άγιος Νικόλαος Κρήτη 72100
2841026182
6032607174

Τετάρτη 27 Φεβρουαρίου 2019

Epigallocatechin‐3‐gallate inhibits proliferation and induces apoptosis in odontogenic keratocyst keratinocytes

Abstract

Objective

The aim of this study was to investigate the effects of epigallocatechin‐3‐gallate on the proliferation and apoptosis of odontogenic keratocyst keratinocytes in vitro.

Materials and Methods

Keratinocytes isolated from the epithelial lining of the odontogenic keratocyst 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 CCK‐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 were used as the control.

Results

The odontogenic keratocyst 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 G1 phase, and induced apoptosis of odontogenic keratocyst keratinocytes. FZD3 and JNK3 were overexpressed in odontogenic keratocyst keratinocytes compared with human oral keratinocytes and were downregulated by epigallocatechin‐3‐gallate treatment.

Conclusion

Epigallocatechin‐3‐gallate inhibited proliferation and induced apoptosis in odontogenic keratocyst keratinocytes, possibly by suppressing the WNT/JNK signalling pathway. It may thus be potentially used for odontogenic keratocyst treatment.

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