Exosomes derived from human bone marrow mesenchymal stem cells promote tumor growth in vivo

被引：370

作者：

Zhu, Wei ^{[1
]}

Huang, Ling ^{[1
]}

Li, Yahong ^{[1
]}

Zhang, Xu ^{[1
]}

Gu, Jianmei ^{[1
]}

Yan, Yongmin ^{[1
]}

Xu, Xiaomeng ^{[1
]}

Wang, Mei ^{[1
]}

Qian, Hui ^{[1
]}

Xu, Wenrong ^{[1
,2
]}

机构：

[1] Jiangsu Univ, Sch Med Sci & Lab Med, Zhenjiang 212013, Jiangsu, Peoples R China

[2] Jiangsu Univ, Affiliated Hosp, Dept Clin Lab Med, Zhenjiang 212013, Jiangsu, Peoples R China

来源：

CANCER LETTERS | 2012年 / 315卷 / 01期

基金：

中国国家自然科学基金;

关键词：

Mesenchymal stem cell; Exosome; Tumor growth; Xenograft model; MAPK pathway; SIGNALING PATHWAY; BREAST-CANCER; CYCLIN D1; VEGF; CONTRIBUTES; METASTASIS; ACTIVATION; EXPRESSION; ANGIOGENESIS; PROGRESSION;

D O I：

10.1016/j.canlet.2011.10.002

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Mesenchymal stem cells (MSCs) can promote tumor growth in a mouse xenograft model, but the exact mechanism remains unclear. In this study, we investigated the effects of bone marrow MSC-derived exosomes (MSC-exosomes) on tumor growth in vitro and in vivo. Our results showed that MSC-exosomes promoted tumor growth in vivo. MSC-exosomes enhanced vascular endothelial growth factor (VEGF) expression in tumor cells by activating extracellular signal-regulated kinase1/2 (ERK1/2) pathway. Inhibition of ERK1/2 activation reserved the increase of VEGF level by MSC-exosomes. Our findings demonstrate a new mechanism through which MSC-exosome-mediated cell-cell interactions may contribute to tumor progression. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

引用

页码：28 / 37

页数：10

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