Abstract
We investigated the antiproliferative effects of the cytoplasmic fraction of Lactococcus lactis ssp. lactis (L.lac CF) on the SNU-1 human stomach cancer cell line. The proliferation of SNU-1 cells was inhibited by treatment with L.lac CF in a time- and dose-dependent manner. L.lac CF caused G0/G1 cell cycle arrest, which was associated with an increase in p53 and p21 expression, the reduction of cyclin D1 expression, and retinoblastoma protein phosphorylation. L.lac CF induced apoptosis in SNU-1 cells, as demonstrated by increased nucleus condensation and a sub-G1 peak. Caspase-3 activation, the induction of p53, and the downregulation of Bcl-2 were also observed in L.lac CF-treated cells. Thus, the inhibitory effect of L.lac CF on SNU-1 cell growth is mainly attributable to the induction of G0/G1 cell cycle arrest and apoptosis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / drug effects*
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Biological Factors / chemistry
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Biological Factors / pharmacology*
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Blotting, Western
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Caspase 3 / metabolism
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Cell Cycle / drug effects*
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Cell Line, Tumor
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Cell Proliferation / drug effects*
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Cell Survival / drug effects
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Cyclin D1 / metabolism
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Cyclin-Dependent Kinase Inhibitor p21 / metabolism*
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Dose-Response Relationship, Drug
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Flow Cytometry
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G1 Phase / drug effects
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Humans
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Lactococcus lactis / chemistry*
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Phosphorylation / drug effects
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Resting Phase, Cell Cycle / drug effects
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Retinoblastoma Protein / metabolism
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Stomach Neoplasms / metabolism
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Stomach Neoplasms / pathology
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Time Factors
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Biological Factors
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Cyclin-Dependent Kinase Inhibitor p21
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Retinoblastoma Protein
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Tumor Suppressor Protein p53
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Cyclin D1
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Caspase 3