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Angiotensin-(1-7)Changes Apoptosis-Related Genes Expression in Human Breast Cancer Cell Line T47D

血管紧张素 - (1-7)变更凋亡相关基因在人类乳腺癌细胞系T47D表达

作     者:Cheryl Alecrim Santos Gabriela Soares da Silva Brito Silvana Aparecida Alves Correa de Noronha Samuel Marcos Ribeiro de Noronha Suma Imura Shimuta Clovis Ryiuchi Nakaie Ismael Dale Cotrim Guerreiro da Silva 

作者机构:Department of GynecologyFederal University of Sao PauloSao PauloBrazil Department of SurgeryFederal University of Sao PauloSao PauloBrazil Department of BiophysicsFederal University of Sao PauloSao PauloBrazil 

出 版 物:《Journal of Cancer Therapy》 (癌症治疗(英文))

年 卷 期:2014年第5卷第14期

页      面:1412-1422页

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基  金:supported by grants number 2008/54383-0 2010/03658-9 and 2011/08531-0 from the Sao Paulo Research Foundation(FAPESP)-Brazil 

主  题:Angiotensin-(1-7) Breast Cancer Cells Apoptosis qPCR Array 

摘      要:Angiotensin-(1-7) [Ang-(1-7)] is a heptapeptide of the renin-angiotensin system with vasodilator and anti-proliferative properties. In the present study, we aim to investigate whether Ang-(1-7) induces apoptosis in breast cancer cells and whether the altered expression of apoptosis-related genes is involved in this process. Human breast cell line T47D was treated with angiotensin-(1-7) and angiotensin II (Ang II). Cell proliferation and apoptosis were quantified using hemocytometer and flow cytometry, respectively. The expression of 84 apoptosis-related genes was evaluated through qPCR array. Ang-(1-7), as opposed to Ang II, decreased proliferation and increased apoptosis in T47D cells. Moreover, many pro-apoptotic genes were up-regulated, such as BAK1, BAX, BCL2L1, BID and BIK. In addition, some anti-apoptotic genes as AKT1 and XIAP were down-regulated by heptapeptide. Although a deeper study should be performed, our results support the hypothesis that Ang-(1-7) could change the expression of several genes related to apoptosis, interfering directly in the molecular pathways associated with the survival of breast cancer cells.

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