EGCG induces lung cancer A549 cell apoptosis by regulating Ku70 acetylation

Oncology Reports
Min LiCheng-Ping Hu

Abstract

Lung cancer is the leading cause of cancer-related death worldwide. (-)-Epigallocatechin-3-gallate (EGCG) is a potential chemopreventive and therapeutic agent for lung cancer. Induction of apoptosis was examined using Annexin V/PI double staining flow cytometry. Western blot analysis detected the protein expression of cleaved caspase-3, Bax and Bcl-xL. Co-immunoprecipitation was used to detect the interaction of Ku70-Bax and the acetylation status of Ku70. Treatment of A549 cells with EGCG-induced apoptosis via increased expression of cleaved caspase-3 and Bax, but decreased expression of Bcl-xL. EGCG upregulated the K70 acetylation status of A549 cells and downregulated the interaction of Bax-Ku70 in a concentration- and time-dependent manner. The apoptosis-promoting effect of EGCG on A549 cells was obviously weakened, along with strengthening of the Bax-Ku70 interaction, after pCDNA3.1(+)-Ku70 plasmid and pCDNA3.1(+)-Ku70539/542R plasmid transfection. Our results established a role of EGCG in inducing cell apoptosis by suppressing Bax activity. Regulating Ku70 acetylation by EGCG, that block the interaction between Ku70 and Bax, will result in lung cancer cell apoptosis.

References

Jul 7, 1993·Journal of the National Cancer Institute·C S Yang, Z Y Wang
Jan 15, 2002·Cardiology Clinics·Q L DeverauxJ C Reed
Sep 3, 2002·Proceedings of the National Academy of Sciences of the United States of America·Yao-Ping LuAllan H Conney
Mar 26, 2003·Nature Cell Biology·Motoshi SawadaShigemi Matsuyama
Mar 26, 2003·Nature Cell Biology·Motoshi SawadaShigemi Matsuyama
Mar 17, 2004·Molecular Cell·Haim Y CohenDavid A Sinclair
Mar 15, 2005·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Kedar HastakMunna L Agarwal
Feb 8, 2011·CA: a Cancer Journal for Clinicians·Ahmedin JemalDavid Forman
May 26, 2011·Journal of Cellular and Molecular Medicine·Oana TudoranIoana Berindan-Neagoe
Dec 14, 2011·European Journal of Cancer : Official Journal for European Organization for Research and Treatment of Cancer (EORTC) [and] European Association for Cancer Research (EACR)·Jane L HurwitzDaniel B Longley
Jan 13, 2012·CA: a Cancer Journal for Clinicians·Lawrence H KushiUNKNOWN American Cancer Society 2010 Nutrition and Physical Activity Guidelines Advisory Committee
Oct 4, 2014·Journal of Cell Death·Manila Hada, Roland Ps Kwok

❮ Previous
Next ❯

Citations

Apr 20, 2018·Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire·Emma Bondy-ChorneyMichael Downey
Jun 25, 2016·Expert Opinion on Therapeutic Patents·Leewanshi ChakrawartiReema Gabrani
Jan 8, 2020·Horticulture Research·En-Hua XiaXiao-Chun Wan
Jul 6, 2019·Anti-cancer Agents in Medicinal Chemistry·Plabon K DasFarhadul Islam
Jul 15, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Saleh A AlmatroodiArshad Husain Rahmani
Mar 10, 2018·Frontiers in Plant Science·Shihua ZhangXiaochun Wan
Nov 17, 2020·Frontiers in Oncology·Shiqin LiHan-Xiang An
Jan 1, 2021·Horticulture Research·En-Hua XiaXiao-Chun Wan
Oct 16, 2021·Frontiers in Pharmacology·Tingyu PanHailang He

❮ Previous
Next ❯

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis