Molecular mechanism of gd@c-82(oh)(22) increasing collagen expression: implication for encaging tumor
文献类型:期刊论文
作者 | Liu, Jing1,2; Kang, Seung-gu3; Wang, Peng1,2; Wang, Yue1,2; Lv, Xiaonan1,2; Liu, Ying1,2; Wang, Fei7; Gu, Zonglin4,5; Yang, Zaixing4,5; Weber, Jeffrey K.3 |
刊名 | Biomaterials
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出版日期 | 2018 |
卷号 | 152页码:24-36 |
关键词 | Cancer therapeutics Fibrosarcoma cells Molecular dynamics Gd-metallofullerenol Tnf receptors Caging cancer cells |
ISSN号 | 0142-9612 |
DOI | 10.1016/j.biomaterials.2017.10.027 |
通讯作者 | Chen, chunying(chenchy@nanoctr.cn) ; Zhou, ruhong(ruhongz@us.ibm.com) ; Zhao, yuliang(zhaoyuliang@ihep.ac.cn) |
英文摘要 | Gadolinium -containing fullerenol gd@c-82(oh)(22) has demonstrated low-toxicity and highly therapeutic efficacy in inhibiting tumor growth and metastasis through new strategy of encaging cancer, however, little is known about the mechanisms how this nanoparticle regulates. fibroblast cells to prison (instead of poison) cancer cells. here, we report that gd@cs-2(oh)(22) promote the binding activity of tumor necrosis factor (tnfa) to tumor necrosis factor receptors 2 (tnfr2), activate tnfr2/p38 mapk signaling pathway to increase cellular collagen expression in fibrosarcoma cells and human primary lung cancer associated fibroblasts isolated from patients. we also employ molecular dynamics simulations to study the atomic-scale mechanisms that dictate how gd@c-82(oh)(22) mediates interactions between tnfot and tnfrs. our data suggest that gd@c-82(oh)(22) might enhance the association between tnr and tnfr2 through a "bridge-like" mode of interaction; by contrast, the fullerenol appears to inhibit tnf alpha-tnfr1 association by binding to two of the receptor's cysteine-rich domains. in concert, our results uncover a sequential, systemic process by which gd@c-82(oh)(22) acts to prison tumor cells, providing new insights into principles of designs of cancer therapeutics. (c) 2017 elsevier ltd. all rights reserved. |
WOS关键词 | NECROSIS-FACTOR-ALPHA ; HUMAN DERMAL FIBROBLASTS ; MESSENGER-RNA LEVELS ; HEPATOCELLULAR-CARCINOMA ; FULLERENE DERIVATIVES ; GENE-TRANSCRIPTION ; PULMONARY-FIBROSIS ; FACTOR RECEPTOR ; TNF-ALPHA ; CELLS |
WOS研究方向 | Engineering ; Materials Science |
WOS类目 | Engineering, Biomedical ; Materials Science, Biomaterials |
语种 | 英语 |
WOS记录号 | WOS:000418215200003 |
出版者 | ELSEVIER SCI LTD |
URI标识 | http://www.irgrid.ac.cn/handle/1471x/2177801 |
专题 | 高能物理研究所 |
通讯作者 | Chen, Chunying; Zhou, Ruhong; Zhao, Yuliang |
作者单位 | 1.Natl Ctr Nanosci & Technol China, CAS Key Lab Biomed Effects Nanomat & Nanosafety, Beijing 100190, Peoples R China 2.Natl Ctr Nanosci & Technol China, CAS Ctr Excellence Nanosci, Beijing 100190, Peoples R China 3.IBM Thomas J Watson Res Ctr, Yorktown Hts, NY 10598 USA 4.Soochow Univ, Inst Quantitat Biol & Med, Collaborat Innovat Ctr Radiat Med Jiangsu Higher, SRMP & RAD X, Suzhou 215123, Peoples R China 5.Soochow Univ, Jiangsu Prov Key Lab Radiat Med & Protect, Suzhou 215123, Peoples R China 6.Chinese Acad Sci, Inst Biophys, Beijing 100101, Peoples R China 7.Zhengzhou Univ, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China 8.Med Coll Wisconsin, Dept Pathol, Childrens Res Inst, Div Pediat Pathol, Milwaukee, WI 53226 USA |
推荐引用方式 GB/T 7714 | Liu, Jing,Kang, Seung-gu,Wang, Peng,et al. Molecular mechanism of gd@c-82(oh)(22) increasing collagen expression: implication for encaging tumor[J]. Biomaterials,2018,152:24-36. |
APA | Liu, Jing.,Kang, Seung-gu.,Wang, Peng.,Wang, Yue.,Lv, Xiaonan.,...&Zhao, Yuliang.(2018).Molecular mechanism of gd@c-82(oh)(22) increasing collagen expression: implication for encaging tumor.Biomaterials,152,24-36. |
MLA | Liu, Jing,et al."Molecular mechanism of gd@c-82(oh)(22) increasing collagen expression: implication for encaging tumor".Biomaterials 152(2018):24-36. |
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来源:高能物理研究所
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