Mol. Cells 2010; 30(4): 341~345  DOI: 10.1007/s10059-010-0124-x
Visfatin Stimulates Proliferation of MCF-7 Human Breast Cancer Cells
Jae Geun Kim1,2, Eun Ok Kim1, Bo Ra Jeong1, Young Joo Min2,4, Jeong Woo Park1,2, Eun Sook Kim3, Il Seong Namgoong3, Young Il Kim3, and Byung Ju Lee1,*
1Department of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan 680-749, Korea, 2Biomedical Research Center, College of Medicine, University of Ulsan, Ulsan 682-714, Korea, 3Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 682-714, Korea, 4Division of Hematology and Oncology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 682-714, Korea
Received March 29, 2010; Revised July 7, 2010; Accepted July 9, 2010.; Published online September 10, 2010.
© The Korean Society for Molecular and Cellular Biology. All rights reserved.

Obesity, a condition characterized by increased fat con-tent and altered secretion of adipokines, is a risk factor for postmenopausal breast cancer. Visfatin has recently been established as a novel adipokine that is highly enriched in visceral fat. Here we report that visfatin regulated proliferation of MCF-7 human breast cancer cells. Exogenous administration of recombinant visfatin increased cell proliferation and DNA synthesis rate in MCF-7 cells. Furthermore, visfatin activated G1-S phase cell cycle progression by upregulation of cyclin D1 and cdk2 expression. Visfatin also increased the expression of matrix metalloproteinases 2, matrix metalloproteinases 9, and vascular endothelial growth factor genes, suggesting that it may function in metastasis and angiogenesis of breast cancer. Taken together, these findings suggest that visfatin plays an important role in breast cancer progression.
Keywords: angiogenesis, breast cancer, metastasis, proliferation, visfatin
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