|
KMID : 1034820210170040533
|
|
Molecular & Cellular Toxicology
2021 Volume.17 No. 4 p.533 ~ p.542
|
|
|
Autophagy inhibition contributes to epigallocatechin-3-gallate-mediated apoptosis in papillary thyroid cancer cells
|
|
Bu Ling
Zheng Tingting
Mao Chaoming
Wu Fei
Mou Xiao
Xu Chengcheng
Luo Xuan
Lu Qingyan
Dong Liyang
Wang Xuefeng
|
|
|
Abstract
|
|
|
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.
|
|
|
KEYWORD
|
|
|
Epigallocatechin-3-gallate, Apoptosis, Autophagy, ROS, Papillary thyroid cancer
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|