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

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 G₁ 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.