Epigallocatechin-3-gallate induces autophagy-related apoptosis associated with LC3B II and Beclin expression of bladder cancer cells
- PMID: 33997996
- DOI: 10.1111/jfbc.13758
Epigallocatechin-3-gallate induces autophagy-related apoptosis associated with LC3B II and Beclin expression of bladder cancer cells
Abstract
The incidence of bladder cancer in traditional green tea-consuming countries was dramatically lower than low green tea-consuming countries. Epigallocatechin-3-gallate (EGCG), an active ingredient extracted from green tea, showed effective inhibition of formation and progression of many tumors. However, whether autophagy involved in this tumor-suppression mechanism of EGCG on bladder cancer was still unclear. In this study, we demonstrated low concentration of EGCG-induced proliferation inhibition and increased apoptosis in bladder cancer cell lines (5,637 and T24 cells) indicated by the increased expression of apoptosis-related protein (caspase9, caspase3 and BAX). In addition, low dose of EGCG also regulated autophagy pathway associated protein (LC3B II and Beclin) expression and this autophagy pathway was blocked by PI3K/AKT inhibitor; moreover, knockdown of ATG5 reversed EGCG-induced apoptosis in 5,637 cells, indicating that EGCG might inhibit the bladder cancer through autophagy pathway. Our findings indicated that EGCG should be considered as a novel therapy for bladder cancer treatment by regulating autophagy pathway. PRACTICAL APPLICATIONS: Our research proved EGCG from green tea could be used as an effective anti-tumor ingredient by revealing another mechanism that epigallocatechin-3-Gallate inhibited bladder cancer cells via inducing autophagy-related apoptosis. And green tea could be considered as a kind of tumor-preventing beverage.
Keywords: apoptosis; autophagy; bladder cancer; epigallocatechin-3-gallate.
© 2021 Wiley Periodicals LLC.
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