Lipid-polymer nanoparticles encapsulating curcumin for modulating the vascular deposition of breast cancer cells

被引:71
作者
Palange, Anna L. [1 ,2 ,3 ]
Di Mascolo, Daniele [1 ,2 ,3 ]
Carallo, Claudio [3 ]
Gnasso, Agostino [3 ]
Decuzzi, Paolo [1 ,2 ,3 ]
机构
[1] Houston Methodist Res Inst, Dept Translat Imaging, Houston, TX 77030 USA
[2] Houston Methodist Res Inst, Dept Nanomed, Houston, TX USA
[3] Magna Graecia Univ Catanzaro, Dept Expt & Clin Med, Catanzaro, Italy
基金
美国国家卫生研究院;
关键词
Nanoparticles; Vascular inflammation; Metastasis; Cancer prevention; Cell adhesion; CIRCULATING TUMOR-CELLS; INTERCELLULAR-ADHESION MOLECULE-1; PANCREATIC-CANCER; HYBRID NANOPARTICLES; COLORECTAL-CANCER; ENDOTHELIAL-CELLS; DELIVERY PLATFORM; FLOW CONDITIONS; METASTASIS; THERAPY;
D O I
10.1016/j.nano.2014.02.004
中图分类号
TB3 [工程材料学];
学科分类号
0805 ; 080502 ;
摘要
Vascular adhesion and endothelial transmigration are critical steps in the establishment of distant metastasis by circulating tumor cells (CTCs). Also, vascular inflammation plays a pivotal role in steering CTCs out of the blood stream. Here, long circulating lipid-polymer nanoparticles encapsulating curcumin (NANOCurc) are proposed for modulating the vascular deposition of CTCs. Upon treatment with NANOCurc, the adhesion propensity of highly metastatic breast cancer cells (MDA-MB-231) onto TNF-alpha stimulated endothelial cells (HUVECs) reduces by similar to 70%, in a capillary flow. Remarkably, the CTCs vascular deposition already reduces up to similar to 50% by treating solely the inflamed HUVECs. The CTCs arrest is mediated by the interaction between ICAM-1 on HUVECs and MUC-1 on cancer cells, and moderate doses of curcumin down-regulate the expression of both molecules. This suggests that NANOCurc could prevent metastasis and limit the progression of the disease by modulating vascular inflammation and impairing the CTCs arrest. From the Clinical Editor: In this novel study, lipid nanoparticles encapsulating curcumin were able to prevent metastasis formation and limited the progression of the disease by modulating vascular inflammation and impairing the circulating tumor cells' arrest as a result of down-regulation of ICAM1 and MUC1 in a highly metastatic breast cancer cell line model. (C) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:991 / 1002
页数:12
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