Fullerenol inhibits the cross-talk between bone marrow-derived mesenchymal stem cells and tumor cells by regulating MAPK signaling

被引：23

作者：

Nie, Xin ^{[1
,2
]}

Tang, Jinglong ^{[1
,2
]}

Liu, Ying ^{[1
,2
]}

Cai, Rong ^{[1
,2
]}

Miao, Qing ^{[1
,2
,3
,4
,5
,6
]}

Zhao, Yuliang ^{[1
,2
]}

Chen, Chunying ^{[1
,2
]}

机构：

[1] Univ Chinese Acad Sci, Natl Ctr Nanosci & Technol China, CAS Key Lab Biomed Effects Nanomat & Nanosafety, Beijing, Peoples R China

[2] Univ Chinese Acad Sci, Natl Ctr Nanosci & Technol China, CAS Ctr Excellence Nanosci, Beijing, Peoples R China

[3] Med Coll Wisconsin, Dept Surg, Childrens Res Inst, Div Pediat Surg, 8700 W Wisconsin Ave, Milwaukee, WI 53226 USA

[4] Med Coll Wisconsin, Dept Surg, Childrens Res Inst, Div Pediat Pathol, 8700 W Wisconsin Ave, Milwaukee, WI 53226 USA

[5] Med Coll Wisconsin, Dept Pathol, Div Pediat Surg, Childrens Res Inst, Milwaukee, WI 53226 USA

[6] Med Coll Wisconsin, Dept Pathol, Div Pediat Pathol, Childrens Res Inst, Milwaukee, WI 53226 USA

来源：

NANOMEDICINE-NANOTECHNOLOGY BIOLOGY AND MEDICINE | 2017年 / 13卷 / 06期

基金：

中国国家自然科学基金;

关键词：

Bone marrow-derived mesenchymal stem cells; Fullerenol; 4T1 tumor cells; MAPK signaling; BREAST-CANCER CELLS; NF-KAPPA-B; IN-VIVO; FIBROBLASTS; BIODISTRIBUTION; NANOPARTICLES; TRANSITION; PATHWAYS; ACTIVATION; ERK;

D O I：

10.1016/j.nano.2017.03.013

中图分类号：

TB3 [工程材料学];

学科分类号：

0805 ; 080502 ;

摘要：

The interaction between bone marrow-derived mesenchymal stem cells (BDMSCs) and tumor cells promotes tumor proliferation and metastasis. We found that 4T1 breast cancer cells induced malignant differentiation of BDMSCs and that BDMSCs also affected the growth and metastasis of 4T1 cells. However, when the interaction between BDMSCs and 4T1 cells was attenuated or blocked by C-60(OH)(22) nanoparticles, tumor growth and metastasis were significantly suppressed. The suppression of metastasis depended on the activation of MAPK signals in the BDMSCs, whereas the underlying pathways were related to a broad range of extracellular responses and were modulated by the secretion of multiple cytokines. Interestingly, C-60(OH)(22) regulated the malignantly differentiated BDMSCs via the Erk-and p38-MAPK and its downstream NF-kappa B signal pathway, but in normal BDMSCs regulation occurred only through Erk-and p38-MAPK and not by NF-kappa B activation. This study may provide a novel mechanism for C-60(OH)(22) nanoparticles as an anti-tumor drug. (C) 2017 Elsevier Inc. All rights reserved.

引用

页码：1879 / 1890

页数：12

共 59 条

[1]

Almeida JPM, 2011, NANOMEDICINE-UK, V6, P815, DOI [10.2217/NNM.11.79, 10.2217/nnm.11.79]

[2]

[Anonymous], TIMES ARCHITECTURE

[3] Bone marrow-derived mesenchymal stem cells and the tumor microenvironment [J].