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논문 기본 정보

자료유형
학술저널
저자정보
Sharifi, Simin (Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences) Barar, Jaleh (Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences) Hejazi, Mohammad Saeid (Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences) Samadi, Nasser (Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제20호
발행연도
2014.1
수록면
8,617 - 8,622 (6page)

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The goal of this study was to establish paclitaxel resistant MCF-7 cells, as in vitro model, to identify the molecular mechanisms leading to acquired chemoresistance in breast cancer cells. Resistant cells were developed by stepwise increasing exposure to paclitaxel. Gene expression levels of Bax and Bcl-2 along with protein levels of caspase-8 and caspase-9 were evaluated in two resistant cell lines (MCF-7/Pac64 and MCF-7/Pac5 nM). Morphological modifications in paclitaxel resistance cells were examined by light microscopy and fluorescence activated cell sorting (FACS). As an important indicator of resistance to chemotheraputic agents, the Bcl-2/Bax ratio showed a significant increase in both MCF-7/Pac5nM and MCF-7/Pac 64nM cells (p<0.001), while caspase-9 levels were decreased (p<0.001) and caspase-8 was increased (p<0.001). FACS analysis demonstrated that MCF-7/Pac64 cells were smaller than MCF-7 cells with no difference in their granularity. Our results support the idea that paclitaxel induces apoptosis in a mitochondrial-dependent manner. Identifying breast cancer patients with a higher Bcl-2/Bax ratio and caspase 9 level and then inhibiting the activity of these proteins may improve the efficacy of chemotheraputic agents.

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