4.7 Article

Diallyl sulfide, diallyl disulfide, and diallyl trisulfide inhibit migration and invasion in human colon cancer colo 205 cells through the inhibition of matrix metalloproteinase-2,-7, and-9 expressions

Journal

ENVIRONMENTAL TOXICOLOGY
Volume 28, Issue 9, Pages 479-488

Publisher

WILEY
DOI: 10.1002/tox.20737

Keywords

DAS; DADS; DATS; migration and invasion; colo 205 human colon cancer cells

Funding

  1. National Science Council, Taiwan [NSC 95-2320-B-039-030-MY2]
  2. Taiwan Department of Health Clinical Trial and Research Center of Excellence [DOH100-TD-B-111-004]
  3. China Medical University Beigang Hospital [CMUBH R100001]

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Diallyl sulfide (DAS), diallyl disulfide (DADS), and diallyl trisulfide (DATS) are major organosulfur compounds exiting in garlic (Allium sativum). These compounds are reported to exhibit various pharmacological properties such as antibacteria, antiangiogenesis, anticancer, and anticoagulation, and they also induce cytotoxicity and induction of apoptosis in human cancer cells. Although these compounds show wide spectrum of biological activities, there are no reports to show that DAS, DADS, and DATS affected migration and invasion of human colon cancer cells, and their exact molecular mechanisms are not well investigated. Therefore, the purpose of this study was to determine whether DAS, DADS, and DATS affected the invasion and migration abilities of colo 205 human colon cancer cells. The results indicate that DAS, DADS, and DATS at 10 and 25 M inhibited the migration and invasion of colo 205 cells in the order of DATS < DADS < DAS. DATS is the highest for inhibition of migration and invasion of colo 205 cells. DAS, DADS, and DATS induce downregulation expression of PI3K, Ras, MEKK3, MKK7, ERK1/2, JNK1/2, and p38 and then lead to the inhibition of MMP-2, -7, and -9. DAS, DADS, and DATS inhibited NF-B and COX-2 for leading to the inhibition of cell proliferation. Taken together, these results demonstrated that application of DAS, DADS, and DATS might serve as potential antimetastatic drugs. (c) 2011 Wiley Periodicals, Inc. Environ Toxicol 28: 479-488, 2013.

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