Resveratrol inhibits cell proliferation and induces apoptosis of human breast carcinoma MCF-7 cells

2004 ◽  
Author(s):  
Young-Ae Kim ◽  
Byung Choi ◽  
Yong Lee ◽  
Dong Park ◽  
Sook-Hee Rhee ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Breast Carcinoma ◽  
Human Breast Carcinoma ◽  
Human Breast ◽  
Mcf 7

scholarly journals In Vitro Study on Apoptosis Induced by Strontium-89 in Human Breast Carcinoma Cell Line

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Cheng Wang ◽  
Jing Wang ◽  
Han Jiang ◽  
Min Zhu ◽  
Baoguo Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Breast Carcinoma ◽  
Transmembrane Potential ◽  
Human Breast Carcinoma ◽  
Inhibition Rate ◽  
Human Breast ◽  
Radioactive Concentration ◽  
Mcf 7

Many radiopharmaceuticals used for medical diagnosis and therapy are beta emitters; however, the mechanism of the cell death caused by beta-irradiation is not well understood. The objective of this study was to investigate the apoptosis of human breast carcinoma MCF-7 cell lines induced by Strontium-89 (89Sr) and its regulation and control mechanism. High-metastatic Breast Carcinoma MCF-7 cells were cultured in vitro using89Sr with different radioactive concentration. The inhibition rate of cell proliferation was measured by MTT color matching method. The cell cycle retardation, apoptosis conditions, mitochondrion transmembrane potential difference and Fas expression were tested and analyzed. The genes P53 and bcl-2 expressions was also analyzed using immunity histochemical analysis. After being induced by89Sr with various of radioactive concentration, it was found that the inhibition of cell proliferation of MCF-7 cells was obviously, the retardation of cell cycle occurred mainly in G2-M. It was also found that the obvious apoptosis occurred after being induced by89Sr, the highest apoptosis rate reached 46.28%. The expressions of Fas acceptor and P53 gene increased, while bcl-2 gene expression decreasesd. These findings demonstrate that in the ranges of a certain radioactive concentration, the inhibition rate of MCF-7 cell proliferation and retardation of cell cycle had positive correlation with the concentration of89Sr. And the mitochondrion transmembrane potential decrease would induce the apoptosis of MCF-7 cell notably, which were controlled by P53 and bcl-2 genes, involved with the Fas acceptor.

scholarly journals Estradiol Exposure Differentially Alters Monolayer versus Microtissue MCF-7 Human Breast Carcinoma Cultures

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0157997 ◽  
Author(s):  
Marguerite M. Vantangoli ◽  
Samantha J. Madnick ◽  
Shelby Wilson ◽  
Kim Boekelheide
Keyword(s):  
Breast Carcinoma ◽  
Human Breast Carcinoma ◽  
Human Breast ◽  
Mcf 7

scholarly journals Phorbol ester selectively stimulates the phospholipase D-mediated hydrolysis of phosphatidylethanolamine in multidrug-resistant MCF-7 human breast carcinoma cells

1994 ◽  
Vol 302 (3) ◽  
pp. 649-654 ◽  
Author(s):  
Z Kiss ◽  
M Tomono ◽  
W B Anderson
Keyword(s):  
Breast Carcinoma ◽  
Phospholipase D ◽  
Multidrug Resistant ◽  
Carcinoma Cells ◽  
Human Breast Carcinoma ◽  
Human Breast ◽  
Breast Carcinoma Cells ◽  
Human Breast Carcinoma Cells ◽  
Hydrolysis Of ◽  
Mcf 7

The phospholipase D (PLD)-mediated synthesis of phosphatidylethanol (PtdEtOH) and the hydrolysis of phosphatidylethanolamine (PtdEtn) and phosphatidylcholine (PtdCho) were examined in drug-sensitive and multidrug-resistant lines of MCF-7 human breast carcinoma cells. In drug-sensitive (MCF-7/WT) cells, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) failed to enhance either the synthesis of PtdEtOH or the hydrolysis of either phospholipid. In the drug-resistant (MCF-7/MDR) cells, 100 nM PMA greatly enhanced both the synthesis of PtdEtOH (approximately 21-fold) and the hydrolysis of PtdEtn (approximately 29-fold), but had no effect on the hydrolysis of PtdCho. The PLD activators sphingosine and H2O2 were found to elicit only a slight (1.28-1.4-fold) stimulatory effect on PtdCho hydrolysis in both the MCF-7/WT and MCF-7/MDR cell types, and had only a small effect on PtdEtn hydrolysis in the MCF-7/WT cells as well. However, these agents significantly (approximately 2.6-3.5-fold) stimulated PtdEtn hydrolysis in the MCF-7/MDR cells. These data indicate that MCF-7/MDR cells contain a PtdEtn-specific PLD activity which can be selectively stimulated by PMA, sphingosine and H2O2.

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