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Functional and molecular effects of a green tea constituent on oral cancer cells
Author(s) -
Belobrov Simone,
Seers Christine,
Reynolds Eric,
Cirillo Nicola,
McCullough Michael
Publication year - 2019
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12914
Subject(s) - cell growth , cancer cell , cancer , downregulation and upregulation , cell culture , cancer research , cell , cell migration , epigallocatechin gallate , chemistry , pharmacology , biology , medicine , biochemistry , polyphenol , antioxidant , genetics , gene
Background Green tea is heavily consumed on a global basis for its health benefits. The active ingredient, (‐)‐epigallocatechin gallate (EGCG), is a major polyphenol demonstrated to inhibit the growth of various non‐oral cancer cell lines and interfere with the carcinogenic process, including downregulation of the epidermal growth factor receptor (EGFR). Our aim was to determine the phenotypic changes of oral cancer cells treated with EGCG and concurrently assess the effect on EGFR expression and activation. Methods Oral cancer cells (H400 and H357) were treated with 10 µg/mL and 20 µg/mL of EGCG for up to 72 hours. Phenotypic changes were assessed by performing cell proliferation analysis and cell migration (Transwell) assays. Expression of EGFR and its phosphorylated form (p‐EGFR) was determined by Western blotting. Results Cell proliferation of both cell lines was significantly reduced at 48hrs when treated with 20 µg/mL EGCG. However, after 72 hours of treatment the effect of EGCG on cell proliferation ceased. Treatment of both cell lines with 10 µg/mL and 20 µg/mL of EGCG resulted in significant reduction in cell migration. Mechanistically, EGFR expression did not change significantly after treatment with EGCG; however, there was a reduction in its phosphorylated form. Conclusion EGCG transiently inhibits both cell proliferation and migration of oral cavity cancer cells. This effect is associated with a decrease in the expression of phosphorylated EGFR. It is possible that more frequent bursts of EGCG could result in a persistent and sustained cancer inhibition, but this requires further research for clarification.