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Anticancer effect of Tamarix gallica extracts on human colon cancer cells involves Erk1/2 and p38 action on G2/M cell cycle arrest

Taking into account that oxidative stress is among the factors causing cancer-related death; chemoprevention which consists in using antioxidant substances such as phenolics could prevent cancer formation and progression. In the present study, phenolic contents and antioxidant activities of methanol...

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Published in:Cytotechnology (Dordrecht) 2013-12, Vol.65 (6), p.927-936
Main Authors: Boulaaba, Mondher, Tsolmon, Soninkhishig, Ksouri, Riadh, Han, Junkyu, Kawada, Kiyokazu, Smaoui, Abderrazak, Abdelly, Chedly, Isoda, Hiroko
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Language:English
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Summary:Taking into account that oxidative stress is among the factors causing cancer-related death; chemoprevention which consists in using antioxidant substances such as phenolics could prevent cancer formation and progression. In the present study, phenolic contents and antioxidant activities of methanolic extracts from the halophyte Tamarix gallica shoots were determined. Moreover, the anticancer effect of this species on human colon cancer cells and the likely underlying mechanisms were also investigated. Shoot extracts showed an appreciable total phenolic content (85 mg GAE/g DW) and a high antioxidant activity (IC 50  = 3.3 μg/ml for DPPH test). At 50 and 100 μg/ml, shoot, leaf, and flower extracts significantly inhibited Caco-2 cell growth. For instance, almost all plant part extracts inhibited cell growth by 62 % at the concentration 100 μg/ml. DAPI staining results revealed that these extracts decrease DNA synthesis and confirm their effect on Caco-2 cells proliferation, principally at 100 μg/ml. More importantly, cell mitosis was arrested at G 2 /M phase. The changes in the cell-cycle-associated proteins (cyclin B1, p38, Erk1/2, Chk1, and Chk2) are correlated with the changes in cell cycle distribution. Taken together, our data suggest that T. gallica is a promising candidate species to be used as a source of anticancer biomolecules.
ISSN:0920-9069
1573-0778
DOI:10.1007/s10616-013-9564-4