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S-Allylcysteine reduces breast tumor cell adhesion and invasion
Leslie A Gapter1, Ong Zhan Yuin, Ka-Yun Ng
1Department of Pharmacy, Faculty of Science, National University of Singapore, 18 Science Drive 4, Building S4, Singapore 117543, Republic of Singapore.
Abstract:
Previous studies show that aqueous garlic extract and its derivatives (e.g. S-allylcysteine [SAC]) prevent carcinogen-induced breast tumorigenesis. However, investigations testing the effect of SAC on later stages of breast tumorigenesis and/or metastasis have produced mixed results. Here we show that SAC significantly reduced anchorage-dependent and -independent growth of MDA-MB-231 breast tumor cells in a dose- and time-dependent fashion, and sub-lethal SAC-treatment altered mammary tumor cell adhesion and invasion through components of the extracellular matrix. We provide evidence to suggest increased expression of E-cadherin and reduced MMP-2 expression and activity are partially responsible for inhibition of mammary tumor cell invasion by SAC. Because E-cadherin and MMP-2 are important in cancer metastasis, these results suggest a link between SAC induction of E-cadherin and reduction of MMP2 activity with the inhibition of cell motility and invasion; thus providing evidence that events leading to breast cancer metastasis are repressed by sub-lethal SAC-treatment.
Insights
S-allylcysteine (SAC), a garlic derivative, inhibits breast tumor cell growth and invasion. It achieves this by altering cell adhesion and reducing key proteins involved in cancer metastasis, suggesting a potential therapeutic role.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Aqueous garlic extract and S-allylcysteine (SAC) have shown promise in preventing breast cancer initiation.
- Previous research on SAC's effects on later stages of breast tumorigenesis and metastasis yielded inconsistent results.
Purpose of the Study:
- To investigate the impact of SAC on established breast tumor cell growth, invasion, and metastasis-related molecular mechanisms.
- To determine if SAC affects anchorage-dependent and -independent growth of MDA-MB-231 breast cancer cells.
Main Methods:
- Treatment of MDA-MB-231 breast tumor cells with varying doses and durations of SAC.
- Assessment of cell growth, adhesion, and invasion assays.
- Analysis of E-cadherin and Matrix Metalloproteinase-2 (MMP-2) expression and activity.
Main Results:
- SAC significantly reduced both anchorage-dependent and -independent growth of MDA-MB-231 cells in a dose- and time-dependent manner.
- Sub-lethal SAC treatment altered mammary tumor cell adhesion and invasion.
- SAC increased E-cadherin expression and decreased MMP-2 expression and activity, contributing to reduced cell invasion.
Conclusions:
- SAC effectively inhibits breast tumor cell growth and invasion, potentially by modulating extracellular matrix interactions.
- Increased E-cadherin and reduced MMP-2 activity are key mechanisms by which SAC represses breast cancer cell motility and invasion.
- These findings suggest SAC has the potential to inhibit key events in breast cancer metastasis.
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