Ethanol promotes mammary tumor growth and angiogenesis: the involvement of chemoattractant factor MCP-1

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• 作者：Siying Wang (12) sywang@ahmu.edu.cn
  Mei Xu (1)
  Feifei Li (2)
  Xin Wang (3)
  Kimberly A. Bower (1)
  Jacqueline A. Frank (1)
  Yanmin Lu (2)
  Gang Chen (1)
  Zhuo Zhang (3)
  Zunji Ke (4)
  Xianglin Shi (3)
  Jia Luo (1) jialuo888@uky.edu
• 关键词：Alcohol – ; Angiogenesis – ; Chemokines – ; Metastasis – ; Migration
• 刊名：Breast Cancer Research and Treatment
• 出版年：2012
• 出版时间：June 2012
• 年：2012
• 卷：133
• 期：3
• 页码：1037-1048
• 全文大小：901.9 KB
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• 作者单位：1. Department of Internal Medicine, University of Kentucky College of Medicine, 130 Health Sciences Research Building, 1095 Veterans Drive, Lexington, KY 40536, USA2. Pathophysiological Department, School of Basic Medicine, Anhui Medical University, 69 Mei Shan Road, Hefei, 230032 Anhui, China3. Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536, USA4. Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031 China
• ISSN：1573-7217

文摘

Alcohol consumption is a risk factor for breast cancer in humans. Experimental studies indicate that alcohol exposure promotes malignant progression of mammary tumors. However, the underlying cellular and molecular mechanisms remain unclear. Alcohol induces a pro-inflammatory response by modulating the expression of cytokines and chemokines. Monocyte chemoattractant protein-1 (MCP-1), also known as chemokine (C–C motif) ligand 2, is a pro-inflammatory chemokine implicated in breast cancer development/malignancy. We investigated the role of MCP-1 in alcohol-promoted mammary tumor progression. Using a xenograft model, we demonstrated that alcohol increased tumor angiogenesis and promoted growth/metastasis of breast cancer cells in C57BL/6 mice. Alcohol up-regulated the expression of MCP-1 and its receptor CCR2 in breast cancer cells in vitro and in vivo. Using a three-dimensional tumor/endothelial cell co-culture system, we demonstrated MCP-1 regulated tumor/endothelial cell interaction and promoted tumor angiogenesis. More importantly, MCP-1 mediated alcohol-promoted angiogenesis; an antagonist of the MCP-1 receptor CCR2 significantly inhibited alcohol-stimulated tumor angiogenesis. The CCR2 antagonist abolished ethanol-stimulated growth of mammary tumors in mice. We further demonstrated that MCP-1 enhanced the migration, but not the proliferation of endothelial cells as well as breast cancer cells. These results suggest that MCP-1 plays an important role in ethanol-stimulated tumor angiogenesis and tumor progression.