Wasabi-Derived 6-(Methylsulfinyl)Hexyl Isothiocyanate Induces Apoptosis in Human Breast Cancer by Possible Involvement of the NF-[kappa]B Pathways
6-(methylsulfinyl)hexyl isothiocyanate (6-MSITC) is a bioactive ingredient of wasabi (Wasabia japonica), which is a popular spice in Japan. 6-MSITC has been reported to inhibit the proliferation of breast cancer and melanoma cell lines. We inoculated 30 female Balb-nu/nu mice with MDA-MB-231 or -453...
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Published in | Nutrition and cancer Vol. 66; no. 5; p. 879 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Mahwah
Taylor & Francis Ltd
01.07.2014
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Subjects | |
Online Access | Get full text |
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Summary: | 6-(methylsulfinyl)hexyl isothiocyanate (6-MSITC) is a bioactive ingredient of wasabi (Wasabia japonica), which is a popular spice in Japan. 6-MSITC has been reported to inhibit the proliferation of breast cancer and melanoma cell lines. We inoculated 30 female Balb-nu/nu mice with MDA-MB-231 or -453 cells, and orally administered varying concentrations of 6-MSITC for 12 days following tumor growth. The tumor volumes and tumor weights from mice inoculated with MDA-MB-231 cells, and the tumor volumes of MDA-MB-453 cells were significantly inhibited by 6-MSITC on Days 9 and 11 after drug administration. DNA fragmentation, DNA ladder, and caspase 3/7 activity performed in vitro revealed that 6-MSITC induced apoptosis of MDA-MB-231, MDA-MB-453, and MCF-7 cells. Furthermore, nuclear factor-...B (NF-...B) expression in the nuclei and phosphorylation of inhibitor ...Ba (I...Ba) was downregulated by 6-MSITC in a concentration-dependent manner; however, this activity was not observed in MCF-7 cells. Moreover, this downregulation of phosphorylated I...Ba by 6-MSITC in MDA-MB-231 and -453 cells supports its inhibitory effects on NF-...B activity. The expression of phosphorylated AKT (pAKT) reduced by 6-MSITC was confirmed in MDA-MB-231 cells. Thus, we conclude that 6-MITC promotes apoptosis of breast cancer cells by inhibiting NF-kB and therefore releasing its control of the PI3K/AKT pathway. (ProQuest: ... denotes formulae/symbols omitted.) |
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ISSN: | 0163-5581 1532-7914 |