Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress

Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress

Licochalcone A (LicA), a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch, has wide spectrum of pharmacological activities. In this study, the anti-cancer effects and potential mechanisms of LicA in non-small cell lung cancer (NSCLC) cells were studied. LicA decr...

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Main Authors: Chenyu Qiu, Tingting Zhang, Wenxin Zhang, Lina Zhou, Bin Yu, Wei Wang, Zhihong Yang, Zhiguo Liu, Peng Zou, Guang Liang
Format: Article
Language:English
Published: MDPI AG 2017-08-01
Series:International Journal of Molecular Sciences
Subjects:
Licochalcone A
cell cycle arrest
ER stress
lung cancer
apoptosis
Online Access:https://www.mdpi.com/1422-0067/18/8/1761
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spelling doaj-89b3a81e105d4ebb8962d5a5b3ffd55e2020-11-24T21:27:51ZengMDPI AGInternational Journal of Molecular Sciences1422-00672017-08-01188176110.3390/ijms18081761ijms18081761Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER StressChenyu Qiu0Tingting Zhang1Wenxin Zhang2Lina Zhou3Bin Yu4Wei Wang5Zhihong Yang6Zhiguo Liu7Peng Zou8Guang Liang9Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, ChinaLicochalcone A (LicA), a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch, has wide spectrum of pharmacological activities. In this study, the anti-cancer effects and potential mechanisms of LicA in non-small cell lung cancer (NSCLC) cells were studied. LicA decreased cell viability and induced apoptosis in a dose-dependent manner in NSCLC cells. LicA inhibited lung cancer cells growth by blocking cell cycle progression at the G2/M transition and inducing apoptosis. LicA treatment decreased the expression of MDM2, Cyclin B1, Cdc2 and Cdc25C in H460 and A549 cancer cell lines. In addition, LicA induced caspase-3 activation and poly-ADP-ribose polymerase (PARP) cleavage, which displayed features of apoptotic signals. Furthermore, LicA increased the expression of endoplasmic reticulum (ER) stress related proteins, such as p-EIF2α and ATF4. These data provide evidence that LicA has the potential to be used in the treatment of lung cancer.https://www.mdpi.com/1422-0067/18/8/1761Licochalcone Acell cycle arrestER stresslung cancerapoptosis
collection DOAJ
language English
format Article
sources DOAJ
author Chenyu Qiu
Tingting Zhang
Wenxin Zhang
Lina Zhou
Bin Yu
Wei Wang
Zhihong Yang
Zhiguo Liu
Peng Zou
Guang Liang
spellingShingle Chenyu Qiu
Tingting Zhang
Wenxin Zhang
Lina Zhou
Bin Yu
Wei Wang
Zhihong Yang
Zhiguo Liu
Peng Zou
Guang Liang
Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress
International Journal of Molecular Sciences
Licochalcone A
cell cycle arrest
ER stress
lung cancer
apoptosis
author_facet Chenyu Qiu
Tingting Zhang
Wenxin Zhang
Lina Zhou
Bin Yu
Wei Wang
Zhihong Yang
Zhiguo Liu
Peng Zou
Guang Liang
author_sort Chenyu Qiu
title Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress
title_short Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress
title_full Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress
title_fullStr Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress
title_full_unstemmed Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress
title_sort licochalcone a inhibits the proliferation of human lung cancer cell lines a549 and h460 by inducing g2/m cell cycle arrest and er stress
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2017-08-01
description Licochalcone A (LicA), a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch, has wide spectrum of pharmacological activities. In this study, the anti-cancer effects and potential mechanisms of LicA in non-small cell lung cancer (NSCLC) cells were studied. LicA decreased cell viability and induced apoptosis in a dose-dependent manner in NSCLC cells. LicA inhibited lung cancer cells growth by blocking cell cycle progression at the G2/M transition and inducing apoptosis. LicA treatment decreased the expression of MDM2, Cyclin B1, Cdc2 and Cdc25C in H460 and A549 cancer cell lines. In addition, LicA induced caspase-3 activation and poly-ADP-ribose polymerase (PARP) cleavage, which displayed features of apoptotic signals. Furthermore, LicA increased the expression of endoplasmic reticulum (ER) stress related proteins, such as p-EIF2α and ATF4. These data provide evidence that LicA has the potential to be used in the treatment of lung cancer.
topic Licochalcone A
cell cycle arrest
ER stress
lung cancer
apoptosis
url https://www.mdpi.com/1422-0067/18/8/1761
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