國家衛生研究院 NHRI:Item 3990099045/5623
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/5623


    Title: Sesamin inhibits vascular endothelial cell growth and angiogenic activity of lung adenocarcinoma cells
    Authors: Tsai, SC;Liu, YC;Li, CP;Huang, TS;Lee, CC
    Contributors: National Institute of Cancer Research
    Abstract: AIM: Sesamin has been indicated to have antihypertensive, antioxidative and antiinflammatory properties. Angiogenesis is the subsequent event of inflammation during wound healing and tumor progression. To investigate whether or not sesamin exerts anti-angiogenic activity, we examined the effects of sesamin on vascular endothelial cells and on the angiogenic activity of cancer cells. METHODS: Human umbilical vein endothelial cells (HUVECs) were isolated and cultivated for the treatments with sesamin. Cell viabilities and growth curves were determined by microculture tetrazolium test and trypan blue exclusion assay. In vitro wound healing and Matrigel invasion assays were performed to determine the migration and invasion abilities of HUVECs. The level of endothelial cell capillary tube and network formation was used to evaluate the angiogenic activity of human lung adenocarcinoma CL1-5 cells. Northern blot analyses were used to detect matrix metalloproteinase-2 (MMP-2) and VEGF mRNA levels in HUVECs and CL1-5 cells, respectively. Western blot was used to estimate the VEGF protein expression in CL1-5 cells and gelatinase zymography was performed to detect the MMP-2 levels secreted from HUVECs.RESULTS: Sesamin inhibited the growth of HUVECs without causing significant cytotoxicity. Sesamin inhibited HUVECs migrating through the matrigel and inhibited their MMP-2 gene expression and enzyme level. Additionally, we found that sesamin inhibited VEGF-induced HUVEC migration by using the wound healing assay. Sesamin inhibited the VEGF expression in invasive CL1-5 cells. The culture media collected from sesamin-pretreated CL1-5 cells were lost the activity to induce the formation of endothelial cell capillary tube and network if compared with the media from untreated CL1-5 cells.
    Date: 2006
    Relation: Journal of Cancer Molecules. 2006;2(5):199-205.
    Link to: http://mupnet.com/JOCM%202%285%29%20199.htm
    Appears in Collections:[Tze-Sing Huang] Periodical Articles

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