Cardamonin induces ROS-mediated G2/M phase arrest and apoptosis through inhibition of NF-κB pathway in nasopharyngeal carcinoma

Yuting Li; You Qin; Chensu Yang; Haibo Zhang; Yong Li; Bian Wu; Jing Huang; Xiaoshu Zhou; Bo Huang; Kunyu Yang; Gang Wu

doi:10.1038/cddis.2017.407

Cardamonin induces ROS-mediated G2/M phase arrest and apoptosis through inhibition of NF-κB pathway in nasopharyngeal carcinoma

Cell Death Dis. 2017 Aug 31;8(8):e3024. doi: 10.1038/cddis.2017.407.

Authors

Yuting Li¹, You Qin¹, Chensu Yang¹, Haibo Zhang², Yong Li³, Bian Wu¹, Jing Huang¹, Xiaoshu Zhou¹, Bo Huang^{4

5}, Kunyu Yang¹, Gang Wu¹

Affiliations

¹ Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
² Department of Radiotherapy, Zhejiang Province People's Hospital, Hangzhou, Zhejiang, China.
³ Department of Oncology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
⁴ Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
⁵ State Key Laboratory of Medical Molecular Biology and Department of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Abstract

Cardamonin has been demonstrated to have an inhibitory effect in many cancers, but its underlying mechanism remains elusive. Here, we studied, for the first time, the mechanism of cardamonin-induced nasopharyngeal carcinoma cell death both in vitro and in vivo. In our study, we showed that cardamonin inhibited cancer cell growth by inducing G2/M phase cell cycle arrest and apoptosis via accumulation of ROS. NF-κB activation was involved in breaking cellular redox homeostasis. Therefore, our results provided new insight into the mechanism of the antitumor effect of cardamonin, supporting cardamonin as a prospective therapeutic drug in nasopharyngeal carcinoma by modulating intracellular redox balance.

Publication types

Retracted Publication

MeSH terms

Animals
Antineoplastic Agents, Phytogenic / pharmacology*
Apoptosis / drug effects
BH3 Interacting Domain Death Agonist Protein / genetics
BH3 Interacting Domain Death Agonist Protein / metabolism
Carcinoma / drug therapy*
Carcinoma / genetics
Carcinoma / metabolism
Carcinoma / pathology
Cell Line, Tumor
Cell Proliferation / drug effects
Chalcones / pharmacology*
G2 Phase Cell Cycle Checkpoints / drug effects*
Gene Expression Regulation, Neoplastic*
Humans
Mice
Mice, Nude
NF-kappa B / agonists
NF-kappa B / genetics*
NF-kappa B / metabolism
Nasopharyngeal Carcinoma
Nasopharyngeal Neoplasms / drug therapy*
Nasopharyngeal Neoplasms / genetics
Nasopharyngeal Neoplasms / metabolism
Nasopharyngeal Neoplasms / pathology
Reactive Oxygen Species / agonists
Reactive Oxygen Species / metabolism
Signal Transduction
Tumor Suppressor Protein p53 / genetics
Tumor Suppressor Protein p53 / metabolism
Xenograft Model Antitumor Assays
bcl-2-Associated X Protein / genetics
bcl-2-Associated X Protein / metabolism

Substances

Antineoplastic Agents, Phytogenic
BAX protein, human
BH3 Interacting Domain Death Agonist Protein
BID protein, human
Chalcones
NF-kappa B
Reactive Oxygen Species
Tumor Suppressor Protein p53
bcl-2-Associated X Protein
cardamonin