Study on the Inhibitory Effect of Gallocatechin-3-gallate on Laryngeal Cancer Cells by Downregulating Epidermal Growth Factor Receptors
10.13748/j.cnki.issn1007-7693.20232485
- VernacularTitle:表没食子儿茶素没食子酸酯通过下调表皮生长因子受体发挥抑制喉癌细胞的作用机制研究
- Author:
Lihong CHEN
1
;
Chunchun LI
1
;
Jia CHEN
2
;
Jimin SHAO
3
;
Jiang CAO
1
Author Information
1. The Second Affiliated Hospital, Zhejiang University School of Medicine Clinical Research Center
2. The Second Affiliated Hospital, Zhejiang University School of Medicine Department of Otorhinolaryngology, Hangzhou 310009, China
3. Department of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou 310058, China
- Publication Type:Journal Article
- Keywords:
epidermal growth factor receptor ； epigallocatechin-3-gallate； laryngeal carcinoma cell； apoptosis ； autophagy ； cell cycle arrest
- From:
Chinese Journal of Modern Applied Pharmacy
2024;41(5):583-590
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the mechanism of action of epigallocatechin-3-gallate(EGCG) in inhibiting laryngeal cancer cells.
METHODS
The expression of epidermal growth factor receptor(EGFR) in laryngeal cancer cell lines AMC-HN-8, TU686 and TU212 was detected by Western blotting, and the inhibitory effects of cetuximab and EGCG on three laryngeal cancer cells were detected by CCK-8 assay. A lentiviral vector containing EGFR promoter and Luc reporter gene was constructed to generate a TU686-EGFR-Luc cell line that could steadily express Luc activity. Luciferase assay was performed to evaluate the effect of EGCG on the transcription activity of EGFR promoter. Cell cycle and apoptosis of EGCG-treated laryngeal carcinoma cells were analyzed by flow cytometry, and changes of the levels of EGFR and downstream ERK1/2, cell cycle-associated proteins P53 and P27, apoptosis-associated proteins BCL2 and PART, and autophagy marker LC3A/B were further examined.
RESULTS
The laryngeal carcinoma cell lines were insensitive to cetuximab but could be effectively suppressed by EGCG. EGCG effectively inhibited the transcription activity of EGFR promoter. Treatment of TU686 cells at sub-IC50 dose EGCG resulted in significant cell cycle arrest at S phase with partial apoptosis. Significant inhibition of expression and activation of EGFR and downstream signaling pathway were observed.
CONCLUSION
EGCG can effectively downregulate EGFR and suppress laryngeal carcinoma cells, further investigation on in vivo effect and mechanisms are anticipated.
