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        Autophagy inhibition contributes to epigallocatechin-3-gallate-mediated apoptosis in papillary thyroid cancer cells

        Bu Ling,Zheng Tingting,Mao Chaoming,Fei Wu,Mou Xiao,Xu Chengcheng,Luo Xuan,Lu Qingyan,Dong Liyang,Wang Xuefeng 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.4

        Background Epigallocatechin-3-gallate is a natural polyphenolic compound that induces apoptosis in papillary thyroid cancer cells. However, its underlying molecular mechanism was not completely clarified. Objectives The present study demonstrated the role of apoptosis and autophagy in EGCG-treated papillary thyroid cancer cells and the relationship between these processes. Results EGCG significantly suppressed the viability of TPC-1 papillary thyroid cancer cells at an IC50 of 17.2 μM. EGCG induced TPC-1 cell apoptosis and cell cycle arrest at S phase and downregulated the protein expression of cyclin A and cyclin-dependent kinase-2. EGCG decreased reactive oxygen species levels, upregulated Bax expression, downregulated Bcl-2 expression and increased cytochrome C levels in the cytosol. Treatment with EGCG also increased the levels of cleaved caspase 3, cleaved caspase 9 and cleaved poly(ADP-ribose) polymerase. EGCG induced an autophagic response via the upregulation of the autophagy-related protein LC3-II and suppression of the AKT/mTOR signalling pathway. Autophagy inhibition further enhanced EGCG-induced cell apoptosis and ROS suppression, which indicated that autophagy played a cytoprotective role in EGCG-treated TPC-1 cells. Conclusion Taken together, these results demonstrated that autophagy inhibition was beneficial to EGCG–mediated apoptosis in papillary thyroid cancer cells. Background Epigallocatechin-3-gallate is a natural polyphenolic compound that induces apoptosis in papillary thyroid cancer cells. However, its underlying molecular mechanism was not completely clarified. Objectives The present study demonstrated the role of apoptosis and autophagy in EGCG-treated papillary thyroid cancer cells and the relationship between these processes. Results EGCG significantly suppressed the viability of TPC-1 papillary thyroid cancer cells at an IC50 of 17.2 μM. EGCG induced TPC-1 cell apoptosis and cell cycle arrest at S phase and downregulated the protein expression of cyclin A and cyclin-dependent kinase-2. EGCG decreased reactive oxygen species levels, upregulated Bax expression, downregulated Bcl-2 expression and increased cytochrome C levels in the cytosol. Treatment with EGCG also increased the levels of cleaved caspase 3, cleaved caspase 9 and cleaved poly(ADP-ribose) polymerase. EGCG induced an autophagic response via the upregulation of the autophagy-related protein LC3-II and suppression of the AKT/mTOR signalling pathway. Autophagy inhibition further enhanced EGCG-induced cell apoptosis and ROS suppression, which indicated that autophagy played a cytoprotective role in EGCG-treated TPC-1 cells. Conclusion Taken together, these results demonstrated that autophagy inhibition was beneficial to EGCG–mediated apoptosis in papillary thyroid cancer cells.

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