title: Wedelia chinensis inhibits nasopharyngeal carcinoma CNE-1 cell growth by inducing G2/M arrest in a Chk1-dependent pathway.
abstract: 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.
authors.affiliation: Institute of Pharmaceutical Bioactive Substances, Guangdong Pharmaceutical University, Guangzhou, P. R. China , Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances, Guangdong Pharmaceutical University, Guangzhou, P. R. China , School of Basic Courses, Guangdong Pharmaceutical University, Guangzhou, P. R. China , School of Pharmaceutical Science, Southern Medical University, Guangzhou, P. R. China.
authors.forename: Manyu
authors.initials: M
authors.lastname: Liu
authors.forename: Weizhang
authors.initials: W
authors.lastname: Wang
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Li
authors.forename: Dayu
authors.initials: D
authors.lastname: Shi
authors.forename: Hanfang
authors.initials: H
authors.lastname: Mei
authors.forename: Xiaobao
authors.initials: X
authors.lastname: Jin
authors.forename: Jiayong
authors.initials: J
authors.lastname: Zhu
mesh_terms: D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics; D002277:Carcinoma; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D000071877:Checkpoint Kinase 1; D059565:G2 Phase Cell Cycle Checkpoints / Q000187:drug effects*; D015870:Gene Expression / Q000187:drug effects; D020868:Gene Silencing; D016259:Genes, myc / Q000235:genetics; D006801:Humans; D058990:Molecular Targeted Therapy; D000077274:Nasopharyngeal Carcinoma; D009303:Nasopharyngeal Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use; D011494:Protein Kinases / Q000235:genetics* / Q000502:physiology*; D034622:RNA Interference; D015398:Signal Transduction / Q000235:genetics* / Q000502:physiology*; D031209:Wedelia
chemical_list: D010936:Plant Extracts; D011494:Protein Kinases; C000605867:CHEK1 protein, human; D000071877:Checkpoint Kinase 1