| Autor: |
Santos RA; Laboratory for Studies of Interactions between Nutrition and Genetics, Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro 20550-013, Brazil., Andrade EDS; Laboratory for Studies of Interactions between Nutrition and Genetics, Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro 20550-013, Brazil., Monteiro M; Laboratory of Functional Foods, Institute of Nutrition Josué de Castro, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil., Fialho E; Laboratory of Functional Foods, Institute of Nutrition Josué de Castro, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil., Silva JL; National Institute of Science and Technology for Structural Biology and Bioimaging, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil., Daleprane JB; Laboratory for Studies of Interactions between Nutrition and Genetics, Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro 20550-013, Brazil., Ferraz da Costa DC; Laboratory for Studies of Interactions between Nutrition and Genetics, Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro 20550-013, Brazil. |
| Abstrakt: |
Green tea (GT) has been shown to play an important role in cancer chemoprevention. However, the related molecular mechanisms need to be further explored, especially regarding the use of GT extract (GTE) from the food matrix. For this study, epigallocatechin gallate (EGCG) and epigallocatechin (EGC) were identified in GTE, representing 42 and 40% of the total polyphenols, respectively. MDA-MB-231 (p53-p.R280K mutant) and MCF-7 (wild-type p53) breast tumor cells and MCF-10A non-tumoral cells were exposed to GTE for 24-48 h and cell viability was assessed in the presence of p53 inhibitor pifithrin-α. GTE selectively targeted breast tumor cells without cytotoxic effect on non-tumoral cells and p53 inhibition led to an increase in viable cells, especially in MCF-7, suggesting the involvement of p53 in GTE-induced cytotoxicity. GTE was also effective in reducing MCF-7 and MDA-MD-231 cell migration by 30 and 50%, respectively. An increment in p53 and p21 expression stimulated by GTE was observed in MCF-7, and the opposite phenomenon was found in MDA-MB-231 cells, with a redistribution of mutant-p53 from the nucleus and no differences in p21 levels. All these findings provide insights into the action of GTE and support its anticarcinogenic potential on breast tumor cells. |
