Visfatin Stimulates Proliferation of MCF-7 Human Breast Cancer Cells
Visfatin Stimulates Proliferation of MCF-7 Human Breast Cancer Cells
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DOI：
10.1007/s10059-010-0124-x
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发表时间：
2010-10-01
影响因子：
3.8
通讯作者：
Lee, Byung Ju
中科院分区：
文献类型：
--
作者：
Kim, Jae Geun;Kim, Eun Ok;Lee, Byung Ju
肥胖是一种以脂肪含量增加和脂肪因子分泌改变为特征的疾病，是绝经后乳腺癌的危险因素。内脏脂肪素是近年来发现的一种新的脂肪因子，在内脏脂肪中高度富集。在这里，我们报告内脂素调节MCF-7人乳腺癌细胞的增殖。外源性重组内脂素可促进MCF-7细胞增殖和DNA合成。内脂素通过上调cyclin D1和cdk 2的表达，激活G1-S期细胞周期进程。内脂素还增加了基质金属蛋白酶2、基质金属蛋白酶9和血管内皮生长因子基因的表达，提示内脂素可能在乳腺癌的转移和血管生成中起作用。综上所述，这些发现表明内脂素在乳腺癌进展中起着重要作用。
Obesity, a condition characterized by increased fat content 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.