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

Abstract

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. Experimental study. 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. 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. Taken together, EGCG inhibits cell proliferation and induces apoptosis via suppression of the EGFR/ERK pathway and cyclin B1/CDK1 complex in ATC cells.