Chamaejasmenin B, a novel candidate, inhibits breast tumor metastasis by rebalancing TGF-beta paradox
文献类型：期刊论文
| 作者 | Wang, Xiaomin2; Li, Qi1; Wang, Yajie1; Xiao, Hongbin3; Li, Yujie1; Kan, Xiaoxi1; Zhang, Ganlin2; Wang, Zhixin3; Yang, Qing1; Chen, Xi1 |
| 刊名 | ONCOTARGET
 |
| 出版日期 | 2016-07-26 |
| 卷号 | 7期号:30页码:48180-48192 |
| 关键词 | Chamaejasmenin b Tumor Metastasis Tgf-beta Paradox Epithelial-mesenchymal Transition Tumor Microenvironment |
| ISSN号 | 1949-2553 |
| DOI | 10.18632/oncotarget.10193 |
| 文献子类 | Article |
| 英文摘要 | Metastasis is the leading lethal factor severely restraining the effectiveness of clinical treatment. TGF-beta is the key regulator for metastasis and influences paradoxically on cancer progression. The known TGF-beta blockers exert little selectivity on its functions, indiscriminately causing the anti-metastatic and pro-growth effects. Under such circumstances, specifically rebalancing the oncological function of TGFbeta provides a crucial oncotarget against metastasis. In our study, we established the screening platform targeting cell motility and identified a potential flavonoid, Chamaejasmenin B (ICJ), extracted from Stellera chamaejasme L..It suppressed the migration and invasion in breast cancer cells in vitro. Moreover, by dynamical quantification of breast cancer progression in small-animal imaging system, ICJ was proved to be a potent inhibitor of metastasis with minimal toxic side effects. Mechanism study further revealed that ICJ efficiently blocked TGF-beta induced EMT, disrupted the interaction between beta 3 integrin-T beta RII complex and, consequently, resulted in the selective inhibition of FAK:Src:p38 pathway. Meanwhile, specific blockage of this pathway largely attenuated the anti-metastatic function of ICJ. Importantly, in contrast with the antagonistic effects on TGF-beta induced metastasis, ICJ obviously sensitized its cytostatic activity, suggesting that it was not a pan-blocker but a rebalancer for the functional output of TGF-beta. Collectively, by targeting TGF-beta Paradox, we experimentally provided a promising candidate for metastatic intervention. |
| WOS关键词 | EPITHELIAL-MESENCHYMAL TRANSITIONS ; GROWTH-FACTOR-BETA ; CANCER METASTASIS ; PROGRESSION ; CELLS ; TUMORIGENESIS ; METHYLATION ; EXPRESSION ; INTEGRIN ; INVASION |
| WOS研究方向 | Oncology ; Cell Biology |
| 语种 | 英语 |
| WOS记录号 | WOS:000385413000106 |
| 出版者 | IMPACT JOURNALS LLC |
| 源URL | [http://cas-ir.dicp.ac.cn/handle/321008/169950]  |
| 专题 | 大连化学物理研究所_中国科学院大连化学物理研究所 |
| 通讯作者 | Zhu, Xiaoxin |
| 作者单位 | 1.China Acad Chinese Med Sci, Inst Chinese Mat Med, Beijing 100700, Peoples R China 2.Capital Med Univ, Beijing Hosp TCM, Beijing 100010, Peoples R China 3.Chinese Acad Sci, Dalian Inst Chem Phys, Key Lab Separat Sci Analyt Chem, Dalian 116023, Peoples R China |
| 推荐引用方式 GB/T 7714 | Wang, Xiaomin,Li, Qi,Wang, Yajie,et al. Chamaejasmenin B, a novel candidate, inhibits breast tumor metastasis by rebalancing TGF-beta paradox[J]. ONCOTARGET,2016,7(30):48180-48192. |
| APA | Wang, Xiaomin.,Li, Qi.,Wang, Yajie.,Xiao, Hongbin.,Li, Yujie.,...&Zhu, Xiaoxin.(2016).Chamaejasmenin B, a novel candidate, inhibits breast tumor metastasis by rebalancing TGF-beta paradox.ONCOTARGET,7(30),48180-48192. |
| MLA | Wang, Xiaomin,et al."Chamaejasmenin B, a novel candidate, inhibits breast tumor metastasis by rebalancing TGF-beta paradox".ONCOTARGET 7.30(2016):48180-48192. |
入库方式： OAI收割
来源：大连化学物理研究所
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