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1.
BMB Rep ; 46(4): 201-6, 2013 Apr.
Article in English | MEDLINE | ID: mdl-23615261

ABSTRACT

Sulforaphane [1-isothiocyanato-4-(methylsulfinyl)-butane] is an isothiocyanate found in some cruciferous vegetables, especially broccoli. Sulforaphane has been shown to display anti-cancer properties against various cancer cell lines. Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in cancer cell invasion. In this study, we investigated the effect of sulforaphane on 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced MMP-9 expression and cell invasion in MCF-7 cells. TPA-induced MMP-9 expression and cell invasion were decreased by sulforaphane treatment. TPA substantially increased NF-κB and AP-1 DNA binding activity. Pre-treatment with sulforaphane inhibited TPA-stimulated NF-κB binding activity, but not AP-1 binding activity. In addition, we found that sulforaphane suppressed NF-κB activation, by inhibiting phosphorylation of IκB in TPA-treated MCF-7 cells. In this study, we demonstrated that the inhibition of TPA-induced MMP-9 expression and cell invasion by sulforaphane was mediated by the suppression of the NF-κB pathway in MCF-7 cells.


Subject(s)
Anticarcinogenic Agents/pharmacology , Matrix Metalloproteinase 9/metabolism , NF-kappa B/metabolism , Signal Transduction/drug effects , Thiocyanates/pharmacology , Carcinogens/toxicity , Cell Movement/drug effects , Humans , I-kappa B Kinase/metabolism , Isothiocyanates , MCF-7 Cells , Phosphorylation , Sulfoxides , Tetradecanoylphorbol Acetate/toxicity , Transcription Factor AP-1/metabolism
2.
J Breast Cancer ; 14(1): 8-13, 2011 Mar.
Article in English | MEDLINE | ID: mdl-21847388

ABSTRACT

PURPOSE: Chemotherapies for breast cancer generally have strong cellular cytotoxicity and severe side effects. Thus, significant emphasis has been placed on combinations of naturally occurring chemopreventive agents. Silibinin is a major bioactive flavonolignan extracted from milk thistle with chemopreventive activity in various organs including the skin, prostate, and breast. However, the mechanism underlying the inhibitory action of silibinin in breast cancer has not been completely elucidated. Therefore, we investigated the effect of silibinin in MCF-7 human breast cancer cells and determined whether silibinin enhances ultraviolet (UV) B-induced apoptosis. METHODS: The effects of silibinin on MCF-7 cell viability were determined using the MTT assay. The effect of silibinin on PARP cleavage, as the hallmark of apoptotic cell death, and p53 protein expression in MCF-7 cells was analyzed using Western blot. The effect of silibinin on UVB-induced apoptosis in MCF-7 cells was analyzed by flow cytometry. RESULTS: A dose- and time-dependent reduction in viability was observed in MCF-7 cells treated with silibinin. Silibinin strongly induced apoptotic cell death in MCF-7 cells, and induction of apoptosis was associated with increased p53 expression. Moreover, silibinin enhanced UVB-induced apoptosis in MCF-7 cells. CONCLUSION: Silibinin induced a loss of cell viability and apoptotic cell death in MCF-7 cells. Furthermore, the combination of silibinin and UVB resulted in an additive effect on apoptosis in MCF-7 cells. These results suggest that silibinin might be an important supplemental agent for treating patients with breast cancer.

3.
Biochem Biophys Res Commun ; 405(4): 552-7, 2011 Feb 25.
Article in English | MEDLINE | ID: mdl-21262201

ABSTRACT

Dihydroavenanthramide D (DHAvD) is a synthetic analog to naturally occurring avenanthramide, which is the active component of oat. Previous study demonstrates that DHAvD strongly inhibits activation of nuclear factor-kappa B (NF-κB), which is a major component in cancer cell invasion. The present study investigated whether DHAvD can modulate MMP-9 expression and cell invasion in MCF-7 human breast cancer cells. MMP-9 expression and cell invasion in response to 12-O-tetradecanoylphorbol-13-acetate (TPA) was increased, whereas these inductions were muted by DHAvD. DHAvD also suppressed activation of mitogen-activated protein kinase (MAPK), and MAPK-mediated nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1) activations in TPA-treated MCF-7 cells. The results indicate that DHAvD-mediated inhibition of TPA-induced MMP-9 expression and cell invasion involves the suppression of the MAPK/NF-κB and MAPK/AP-1 pathways in MCF-7 cells. DHAvD may have potential value in breast cancer metastasis.


Subject(s)
Breast Neoplasms/enzymology , Breast Neoplasms/pathology , Matrix Metalloproteinase Inhibitors , ortho-Aminobenzoates/pharmacology , Cell Line, Tumor , Cell Survival/drug effects , Humans , Matrix Metalloproteinase 9/biosynthesis , Mitogen-Activated Protein Kinases/metabolism , Neoplasm Invasiveness , Signal Transduction , Tetradecanoylphorbol Acetate/pharmacology
4.
Int J Mol Med ; 25(2): 255-60, 2010 Feb.
Article in English | MEDLINE | ID: mdl-20043135

ABSTRACT

Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in breast cancer cell invasion. NF-kappaB and AP-1 are known to induce MMP-9 expression. We investigated whether cordycepin, an NF-kappaB or AP-1 inhibitor, can modulate MMP-9 expression and cell invasion in MCF-7 cells. Toxicity of cordycepin was determined by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. MMP-9 expression was determined by real-time PCR, Zymography, and Western blot analysis. AP-1 activation was assayed by electrophoretic mobility shift assay (EMSA). MAPK signaling was evaluated by Western blotting with specific p-ERK, and ERK, p-p38, p38, p-JNK, JNK antibodies. Cordycepin suppressed AP-1 activation, but not NF-kappaB activation in 12-O-tetradecanoylpho-bol-13-acetate (TPA)-treated MCF-7 cells. Cordycepin inhibits TPA-induced MMP-9 expression and cell invasion by suppressing AP-1 activation. Also, cordycepin suppressed the MAPK signaling pathway. Cordycepin is a potent inhibitor of TPA-induced MMP-9 expression and blocks strongly the ability of AP-1 activation via MAPK signaling pathway in MCF-7 cells.


Subject(s)
Antineoplastic Agents/pharmacology , Breast Neoplasms/metabolism , Deoxyadenosines/pharmacology , MAP Kinase Signaling System/drug effects , Matrix Metalloproteinase Inhibitors , Tetradecanoylphorbol Acetate/pharmacology , Transcription Factor AP-1/antagonists & inhibitors , Analysis of Variance , Breast Neoplasms/drug therapy , Breast Neoplasms/enzymology , Breast Neoplasms/pathology , Cell Line, Tumor , Cell Survival/drug effects , Female , Gene Expression/drug effects , Humans , Matrix Metalloproteinase 9/biosynthesis , Matrix Metalloproteinase 9/genetics , NF-kappa B/genetics , NF-kappa B/metabolism , Neoplasm Invasiveness , Polymerase Chain Reaction , Tetradecanoylphorbol Acetate/antagonists & inhibitors , Transcription Factor AP-1/genetics , Transcription Factor AP-1/metabolism
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