Laboratory of Cellular Communication, Program of Cell & Molecular Biology, Institute of Biomedical Sciences (ICBM), Faculty of Medicine, University of Chile, Av. Independencia 1027, Santiago, Chile.
Center for Studies on Exercise Metabolism & Cancer (CEMC), University of Chile, Av. Independencia 1027, Santiago, Chile.
Nanomedicine (Lond). 2018 Jun;13(12):1447-1462. doi: 10.2217/nnm-2017-0390. Epub 2018 Jul 4.
To track early events during lung metastasis, we labeled cells expressing (B16F10) or lacking CAV1 (B16F10) with gold nanoparticles conjugated to the peptide TAT (AuNPs-PEG-TAT).
B16F10 expressing or lacking CAV1 were labeled with AuNPs-PEG-TAT. The physicochemical properties and cytotoxicity of these nanoparticles, as well as their effects on migration and invasiveness of B16F10 cells in vitro were evaluated. Ex vivo lung distribution of the labeled cells after tail vein injection into C57BL/6 mice was examined.
AuNPs-PEG-TAT did not affect B16F10 viability, migration and invasiveness. The metastatic and tumorigenic capability of the labeled B16F10 was also not modified in comparison to unlabeled B16F10 cells. CAV1 expression favored the retention of B16F10 cells in the lungs of mice 2 h post injection, suggesting CAV1 promoted adherence to endothelial cells and transendothelial migration.
We developed a protocol to label B16F10 cells with AuNPs-PEG-TAT that permits subsequent tracking of cells in mice. CAV1 overexpression was found to increase retention and transendothelial migration of B16F10 cells in the lung.
为了追踪肺转移早期事件，我们用金纳米颗粒偶联 TAT 肽（AuNPs-PEG-TAT）对表达（B16F10）或缺乏 CAV1（B16F10）的细胞进行标记。
用 AuNPs-PEG-TAT 标记表达或缺乏 CAV1 的 B16F10。评估这些纳米颗粒的理化性质和细胞毒性，以及它们对 B16F10 细胞体外迁移和侵袭的影响。通过尾静脉注射 C57BL/6 小鼠，检测标记细胞在体外的肺分布。
AuNPs-PEG-TAT 不影响 B16F10 的活力、迁移和侵袭能力。与未标记的 B16F10 细胞相比，标记的 B16F10 的转移和致瘤能力也没有改变。与未标记的 B16F10 细胞相比，CAV1 表达促进了 B16F10 细胞在注射后 2 小时在小鼠肺部的保留，表明 CAV1 促进了与内皮细胞的黏附和跨内皮迁移。
我们开发了一种用 AuNPs-PEG-TAT 标记 B16F10 细胞的方案，允许在小鼠中对细胞进行后续追踪。发现 CAV1 过表达增加了 B16F10 细胞在肺部的保留和跨内皮迁移。
