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논문 기본 정보

자료유형
학술저널
저자정보
Delphi, Ladan (Department of Animal Biology, School of Biology, College of Science, University of Tehran) Sepehri, Houri (Department of Animal Biology, School of Biology, College of Science, University of Tehran) Khorramizadeh, Mohammad Reza (Endocrinology and Metabolic Research Institute, Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences) Mansoori, Fatemeh (Department of Animal Biology, School of Biology, College of Science, University of Tehran)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제16권 제13호
발행연도
2015.1
수록면
5,265 - 5,271 (7page)

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Background: The effects of plant products on cancer cells has become a field of major importance. Many substancesmay induce apoptosis in anti-cancer treatment. Pectins, a family of complex polysaccharides, and their degradation products may for exasmple exert apoptotic effects in cancer cells. Apples and citrus fruits are the main sources of pectin which can be applied for anti-cancer research. The present study concerned an intact form of pectic-oligoshaccharide named pectic acid (poly galactronic acid). Materials and Methods: Inhibition of cell proliferation assays (MTT), light microscopy, fluorescence microscopy (acridin orange/ethidium bromide), DNA fragmentation tests, cell cycle analysis, annexin PI and Western blotting methods were applied to evaluate apoptosis. Results: The results indicated that pectic acid inhibited cell growth and reduced cell attachment after 24h incubation. This did not appear to be due to necrosis, since morphological features of apoptosis were detected with AO/EB staining and cell cycling was blocked in the sub-G1 phase. Annexin/PI and DNA fragmentation findings indicated that apoptosis frequency increased after 24h incubation with pectic acid. In addition, the data showed pectic acid induced caspase-dependent apoptosis. Conclusions: These data indicate that apple pectic acid without any modification could trigger apoptosis in MDA-MB-231 human breast cancer cells and has potential to improve cancer treatment as a natural product.

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