الفهرس 
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Abstract
Breast cancer is the most common disease in women worldwide and it is the most common cancer in the Arab world. It affects women at an early age compared with women in western countries. Doxorubicin (DOX) is a chemotherapeutic drug from anthracycline family and is highly effective in advanced breast cancer. Unfortunately, the toxic effects of DOX affect normal cells as well as cancer cells, which lead to severe heart damage. Many strategies have been investigated to protect the heart against DOX induced cardiotoxicity. Recent studies proved the effect of astaxanthin (AST) as an anti-cancer. Therefore, the present study aimed to study the effect of AST co-treatment with DOX on the growth of MCF-7 breast cancer cell line and investigate the possible mechanism to overcome the side effects and multidrug resistance of Doxorubicin treatment.
Materials and methods: To assess these effects, we investigated the DOX effect on apoptosis induction, cell cycle phase distribution, cellular uptake, ABCB1mRNA gene expression and p-glycoprotein activity in breast cancer cells in presence and absence of AST.
Results: The addition of AST (133 and 250µg/ml) increased the effectiveness of DOX as it led to a significant decrease in IC50 compared to the cells treated with DOX alone. Moreover, flow cytometric analysis of the MCF-7 cells treated with DOX (4.5μg/ml) simultaneously with AST (250μg/ml) showed enhanced arrest of the cells in G0\G1 (35.50 %).In addition, significantly increased apoptotic phase cells to 39.13%when AST (250μg/ml) added to DOX (4.5 µg/ml) compared to 27.3% in DOX alone. AST (133 µg/ml and 250 µg/ml) increased the cellular uptake of DOX significantly by 124.41% and 133.69 % respectively compared to DOX (61.22%) alone. When AST (133 and 250 µg/ml) added to DOX this lead to significantly decreased in Protein expression of ABCB1 (6.6 and 1.2%) respectively compared to DOX alone (74%)
Conclusion: The present study concluded that AST potentiates the cytotoxic activity of DOX against the growth of MCF-7 cancer cells through induction of apoptosis, inhibition of p-glycoprotein activity, enhance DOX cellular uptake and decreased in Protein expression of ABCB1.