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Cucurbitacin I inhibits STAT3, but enhances STAT1 signaling in human cancer cells in vitro through disrupting actin filaments

文献类型：期刊论文

作者Guo, Hui1,2; Kuang, Shan1,2; Song, Qiao-ling1,2; Liu, Man1,2; Sun, Xiao-xiao1,2; Yu, Qiang1,2
刊名ACTA PHARMACOLOGICA SINICA
出版日期2018-03
卷号39期号:3页码:425-437
关键词cucurbitacin I cancer cells STAT1 STAT3 actin phosphorylation
ISSN号1671-4083
DOI10.1038/aps.2017.99
文献子类Article
英文摘要STAT1 and STAT3 are two important members of the STAT (signal transducers and activators of transcription) protein family and play opposing roles in regulating cancer cell growth. Suppressing STAT3 and/or enhancing STAT1 signaling are considered to be attractive anticancer strategies. Cucurbitacin I (CuI) isolated from the cucurbitacin family was reported to be an inhibitor of STAT3 signaling and a disruptor of actin cytoskeleton. In this study we investigated the function and mechanisms of CuI in regulating STAT signaling in human cancer cells in vitro. CuI (0.1-10 mmol/L) dose-dependently inhibited the phosphorylation of STAT3, and enhanced the phosphorylation of STAT1 in lung adenocarcinoma A549 cells possibly through disrupting actin filaments. We further demonstrated that actin filaments physically associated with JAK2 and STAT3 in A549 cells and regulated their phosphorylation through two signaling complexes, the IL-6 receptor complex and the focal adhesion complex. Actin filaments also interacted with STAT1 in A549 cells and regulated its dephosphorylation. Taken together, this study reveals the molecular mechanisms of CuI in the regulation of STAT signaling and in a possible inhibition of human cancer cell growth. More importantly, this study uncovers a novel role of actin and actin-associated signaling complexes in regulating STAT signaling.
WOS关键词BREAST-CANCER ; MESENCHYMAL TRANSITION ; TUMOR-FORMATION ; MELANOMA-CELLS ; CYCLE ARREST ; LUNG-CANCER ; F-ACTIN ; PATHWAY ; ACTIVATION ; EXPRESSION
资助项目China Ministry of Science and Technology Key New Drug Creation and Manufacturing Program[2014ZX9102001002] ; China National Key Basic Research Program[2013CB910900] ; National Natural Science Foundation of China[81373447] ; National Natural Science Foundation of China[81673465]
WOS研究方向Chemistry ; Pharmacology & Pharmacy
语种英语
CSCD记录号CSCD:6174717
WOS记录号WOS:000426844400010
出版者ACTA PHARMACOLOGICA SINICA
源URL[http://119.78.100.183/handle/2S10ELR8/279873]  
专题药理学第一研究室
通讯作者Yu, Qiang
作者单位1.Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China;
2.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
推荐引用方式
GB/T 7714		 Guo, Hui,Kuang, Shan,Song, Qiao-ling,et al. Cucurbitacin I inhibits STAT3, but enhances STAT1 signaling in human cancer cells in vitro through disrupting actin filaments[J]. ACTA PHARMACOLOGICA SINICA,2018,39(3):425-437.
APA Guo, Hui,Kuang, Shan,Song, Qiao-ling,Liu, Man,Sun, Xiao-xiao,&Yu, Qiang.(2018).Cucurbitacin I inhibits STAT3, but enhances STAT1 signaling in human cancer cells in vitro through disrupting actin filaments.ACTA PHARMACOLOGICA SINICA,39(3),425-437.
MLA Guo, Hui,et al."Cucurbitacin I inhibits STAT3, but enhances STAT1 signaling in human cancer cells in vitro through disrupting actin filaments".ACTA PHARMACOLOGICA SINICA 39.3(2018):425-437.

入库方式： OAI收割

来源：上海药物研究所

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