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Evodiamine Suppresses ABCG2 Mediated Drug Resistance by Inhibiting p50/p65 NF‐κB Pathway in Colorectal Cancer
Author(s) -
Sui Hua,
Zhou LiHong,
Zhang YaLi,
Huang JianPing,
Liu Xuan,
Ji Qing,
Fu XiaoLing,
Wen HaoTian,
Chen ZheSheng,
Deng WanLi,
Zhu HuiRong,
Li Qi
Publication year - 2016
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25451
Subject(s) - evodiamine , pharmacology , apoptosis , colorectal cancer , cancer cell , cancer research , nf κb , cancer , chemistry , biology , medicine , biochemistry
ABSTRACT Evodiamine (Evo), extracted from the Chinese herbal medicine Evodia rutaecarpa, has cytotoxic effects on different types of human cancer cells. However, its effects on drug resistance and their molecular mechanism and therapeutic target in colorectal cancer are not well understood. In the present study, we observed that Evo inhibited cell growth and induced apoptosis in adose‐and time‐dependent manner in HCT‐116/L‐OHP cells. Moreover, Evo treatment reduced Rhodamine 123 accumulation and ATPase activity in HCT‐116/L‐OHP cells, indicating that Evo decreased the efflux function in HCT‐116/L‐OHP cells. Interestingly, phosphorylation of NF‐κB pathway, particularly p50/p65, was also inhibited by Evo treatment. Furthermore the effect of Evo in reversing drug resistance and suppressing phosphorylation of NF‐κB pathway were attenuated after treatment with the NF‐κB activator (LPS). Additionally, Evo inhibited the tumor growth in a colorectal MDR cancer xenograft model and down regulated p‐NF‐κB level in vivo. Our study provided the first direct evidence that Evo can attenuate multidrug resistance by blocking p‐NF‐κB signaling pathway in human colorectal cancer. Evo could be a potential candidate for cancer chemotherapy. J. Cell. Biochem. 117: 1471–1481, 2016. © 2015 Wiley Periodicals, Inc.