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Investigation of Gallic Acid Induced Anticancer Effect in Human Breast Carcinoma MCF-7 Cells

Authors

  • Ke Wang,

    Corresponding author
    1. Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, Jiangsu Province, People's Republic of China
    • Correspondence to: Ke Wang.

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  • Xue Zhu,

    1. Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, Jiangsu Province, People's Republic of China
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  • Kai Zhang,

    1. Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, Jiangsu Province, People's Republic of China
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  • Ling Zhu,

    1. Save Sight Institute, University of Sydney, NSW, Australia
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  • Fanfan Zhou

    1. Faculty of Pharmacy, University of Sydney, NSW, Australia
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  • Contract Grant Sponsor: National Natural Science Foundation.

  • Contract Grant Number: 81300787.

  • Contract Grant Sponsor: Natural Science Foundation of Jiangsu Province.

  • Contract Grant Numbers: BK2011168 and BK2012105.

  • Contract Grant Sponsor: Youth Foundation of Jiangsu Institute of Nuclear Medicine.

  • Contract Grant Number: QN201111.

ABSTRACT

Gallic acid (GA), a polyhydroxylphenolic compound abundantly distributed in plants, fruits, and foods, has been reported to have various biological activities including an anticancer effect. In this study, we extensively investigated the anticancer effect of GA in human breast carcinoma MCF-7 cells. Our study indicated that treatment with GA resulted in inhibition of proliferation and induction of apoptosis in MCF-7 cells. Then, the molecular mechanism of GA's apoptotic action in MCF-7 cells was further investigated. The results revealed that GA induced apoptosis by triggering the extrinsic or Fas/FasL pathway as well as the intrinsic or mitochondrial pathway. Furthermore, the apoptotic signaling induced by GA was amplified by cross-link between the two pathways. Taken together, our findings may be useful for understanding the mechanism of action of GA on breast cancer cells and provide new insights into the possible application of such compound and its derivatives in breast cancer therapy.

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