Wedelia chinensis Inhibits Nasopharyngeal Carcinoma CNE-1 Cell Growth by Inducing G2/M Arrest in a Chk1-Dependent Pathway

被引:8
|
作者
Liu, Manyu [1 ,2 ,3 ,6 ]
Wang, Weizhang [2 ,3 ,4 ,5 ]
Li, Xiaobo [1 ,2 ,3 ]
Shi, Dayu [1 ,2 ,3 ]
Mei, Hanfang [1 ,2 ,3 ]
Jin, Xiaobao [1 ,2 ,3 ]
Zhu, Jiayong [1 ,2 ,3 ,6 ]
机构
[1] Guangdong Pharmaceut Univ, Inst Pharmaceut Bioact Subst, Guangzhou 510006, Guangdong, Peoples R China
[2] Guangdong Pharmaceut Univ, Guangdong Prov Key Lab Pharmaceut Bioact Subst, Guangzhou 510006, Guangdong, Peoples R China
[3] Guangdong Pharmaceut Univ, Sch Basic Courses, Guangzhou 510006, Guangdong, Peoples R China
[4] Hlth Ind Sci & Technol Pk Investment Management C, Guangzhou Higher Educ Mega Ctr, Guangzhou, Guangdong, Peoples R China
[5] Southern Med Univ, Sch Publ Hlth & Trop Med, Guangzhou, Guangdong, Peoples R China
[6] Southern Med Univ, Sch Pharmaceut Sci, Guangzhou, Guangdong, Peoples R China
来源
AMERICAN JOURNAL OF CHINESE MEDICINE | 2013年 / 41卷 / 05期
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
Wedelia chinensis; Nasopharyngeal Carcinoma; G2/M Arrest; Chk1; NF-KAPPA-B; ARF TUMOR-SUPPRESSOR; PROSTATE-CANCER; MICROSATELLITE INSTABILITY; TRANSCRIPTIONAL REGULATION; ENDOMETRIAL CANCERS; CHECKPOINT; APOPTOSIS; DEATH; CHK1;
D O I
10.1142/S0192415X1350078X
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Although Wedelia chinensis, an herb in traditional Chinese medicine, has been widely used for the treatment of inflammation, the effects of W. chinensis on cancer cell growth and the related molecular mechanisms behind these effects have largely remained unexplored to date. In the present study, W. chinensis plant extracts were obtained using either ethanol (E), petroleum ether (PE), ethyl acetate (EA) or butyl alcohol (BA). Then, extracts were examined for bioactivity in vitro via MTT assay in five human cancer cell lines. Our results showed that one subfraction of the EA extract (EA6) was cytotoxic to nasopharyngeal carcinoma (NPC) CNE-1 cells, among all cell lines evaluated. Treatment of CNE-1 cells with EA6 resulted in significant G2/M cell cycle arrest and modest apoptosis. EA6 induced Chk1 activation and inhibition of Chk1 in CNE-1 cells by RNA interference (RNAi) markedly abrogated EA6-mediated G2/M arrest and abolished EA6-induced cytotoxicity. EA6 treatment resulted in notable reduction of c-myc expression in CNE-1 cells, whereas silencing Chk1 inhibited such effects of EA6. Our results indicate that Chk1 is a novel molecular target of EA6 in NPC cells and also suggest an intervention strategy for NPC by EA6 exploring its molecular mechanisms of action.
引用
收藏
页码:1153 / 1168
页数:16
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