TY - JOUR ID - 19399 TI - Theaflavin promoted apoptosis in nasopharyngeal carcinoma unexpectedly via inducing autophagy in vitro JO - Iranian Journal of Basic Medical Sciences JA - IJBMS LA - en SN - 2008-3866 AU - Xu, Jing AU - Wang, Shujuan AU - Bu, Shanshan AU - Guo, Xiaoqi AU - Ge, Hong AD - Department of Radiotherapy, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan province, China Y1 - 2022 PY - 2022 VL - 25 IS - 1 SP - 68 EP - 74 KW - Apoptosis KW - Autophagy KW - Nasopharyngeal carcinoma KW - Proliferation KW - Theaflavin DO - 10.22038/ijbms.2021.59190.13143 N2 - Objective(s): This study aimed to investigate the mechanism of the anticancer effect of theaflavin (TF) in nasopharyngeal carcinoma.Materials and Methods: CNE2 cells were used to study the anticancer effect of TF. This study used Cell Counting Kit-8 (CCK8) assay on proliferation and used flow cytometry to detect apoptosis. The protein expression of Bcl-2, Bax, caspase 3, and caspase 9 was detected by Western blot, and autophagy-related proteins were also detected.Results: TF inhibited proliferation of CNE2 cells, promoted apoptosis, and up-regulated the expression of caspase 3, caspase 9, and Bax, and decreased the level of Bcl-2. Unexpectedly, TF induced autophagy rather than inhibiting autophagy through up-regulating the levels of the autophagy marker light chain 3 (LC3) and Lysosomal-associated membrane protein 1 (LAMP1) and reducing levels of the autophagosome cargo protein p62, and the effect was via the mTOR pathway. Besides, autophagy inhibitor Chloroquine (CQ) suppressed the effect of TF on Bax, Bcl-2 and activation of caspase 3 and caspase 9.Conclusion: TF promoted apoptosis of nasopharyngeal carcinoma cells, the mechanism was unexpectedly involved in inducing autophagy. UR - https://ijbms.mums.ac.ir/article_19399.html L1 - https://ijbms.mums.ac.ir/article_19399_5f49498cdcb359725be7ce581f3b90f8.pdf ER -