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Quantitative proteomics characterization on the antitumor effects of isodeoxyelephantopin against nasopharyngeal carcinoma
Author(s) -
Yan GuangRong,
Tan Zilu,
Wang Yang,
Xu ManLi,
Yu Guangchuang,
Li Yaolan,
He QingYu
Publication year - 2013
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.201300152
Subject(s) - stable isotope labeling by amino acids in cell culture , apoptosis , dna damage , inflammation , biology , oxidative stress , proteomics , quantitative proteomics , microbiology and biotechnology , cancer research , chemistry , biochemistry , immunology , gene , dna
Isolated from E lephantopus scaber L ., a C hinese medicinal herb that is widely used to prevent and treat cancers in China, isodeoxyelephantopin ( ESI ) exerted antitumor effects on several cancer cells. However, its antitumor mechanism is still not clear. In this study, we found that ESI could induce G 2/ M arrest and subsequently stimulate cell apoptosis in dose‐ and time‐dependent manners. We used SILAC quantitative proteomics to identify ESI ‐regulated proteins in cancer cells, and found that 124 proteins were significantly altered in expression. Gene ontology and I ngenuity P athway A nalysis revealed that these proteins were mainly involved in the regulation of oxidative stress and inflammation response. Functional studies demonstrated that ESI induced G 2/ M arrest and apoptosis by inducing ROS generation, and that antioxidant N ‐acetyl‐ l ‐cysteine could block the ESI ‐induced antitumor effects. Accumulated ROS resulted in DNA breakage, subsequent G 2/ M arrest and mitochondrial‐mediated apoptosis. ESI upregulated the expression of anticancer inflammation factors IL ‐12a, IFN ‐α, and IFN ‐β through ROS ‐dependent and independent pathways. The current work reveals that ESI exerts its antitumor effects through ROS ‐dependent DNA damage, mitochondrial‐mediated apoptosis mechanism and antitumor inflammation factor pathway.