Epigallocatechin-3-gallate induces growth inhibition and apoptosis of human anaplastic thyroid carcinoma cells through suppression of EGFR/ERK pathway and cyclin B1/CDK1 complex

• Published in: Journal of surgical oncology 2011-12, Vol.104 (7), p.776-780
• Main Authors: Lim, Young Chang, Cha, Yun Yi
• Format: Article
• Language: English
• Subjects: anaplastic carcinoma; Anticarcinogenic Agents - pharmacology; apoptosis; Apoptosis - drug effects; Carcinoma - drug therapy; Catechin - analogs & derivatives; Catechin - pharmacology; CDC2 Protein Kinase - antagonists & inhibitors; Cell Line, Tumor; Cell Proliferation - drug effects; Cyclin B1 - antagonists & inhibitors; EGCG; Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors; Humans; Receptor, Epidermal Growth Factor - antagonists & inhibitors; Signal Transduction - drug effects; thyroid gland; Thyroid Neoplasms - drug therapy
• ISSN: 0022-4790; 1096-9098
• DOI: 10.1002/jso.21999

Background Anaplastic thyroid carcinoma (ATC) is one of the most lethal cancers because of its aggressiveness and the lack of efficacious therapy. Epigallocatechin‐3‐gallate (EGCG), a major catechin in green tea, was shown to possess remarkable therapeutic potential against various types of human cancer cells in in vitro and in vivo models. The aim of this study was to investigate the effect of EGCG on the proliferation and apoptosis of ARO cells—human ATC cells. Study design Experimental study. Methods Human ATC cell line, ARO, was treated with EGCG. Cell viability was assessed by MTT assay. Inhibition of EGFR/MAPK pathway and cell cycle‐related proteins by EGCG were measured by Western blot analysis. In addition, cell cycle analysis was measured by flow cytometry. Results EGCG treatment inhibited the growth of ARO cells in a dose‐dependent manner. Furthermore, EGCG suppressed phosphorylation of EGFR, ERK1/2, JNK, and p38. These changes were associated with increased p21 and reduced cyclin B1/CDK1 expression. In addition, EGCG treatment increased the accumulation of sub‐G1 cell, activated caspase‐3 and cleaved PARP. Conclusions Taken together, EGCG inhibits cell proliferation and induces apoptosis via suppression of the EGFR/ERK pathway and cyclin B1/CDK1 complex in ATC cells. J. Surg. Oncol. 2011; 104:776–780. © 2011 Wiley Periodicals, Inc.