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Genistein Modulates Proliferation and Mitochondrial Functionality in Breast Cancer Cells Depending on ERalpha/ERbeta Ratio
Author(s) -
Pons Daniel Gabriel,
NadalSerrano Mercedes,
BlanquerRossello M. Mar,
SastreSerra Jorge,
Oliver Jordi,
Roca Pilar
Publication year - 2014
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24737
Subject(s) - genistein , estrogen receptor , apoptosis , cell growth , chemistry , estrogen receptor beta , cancer cell , estrogen receptor alpha , medicine , cancer research , endocrinology , biology , cancer , breast cancer , biochemistry
ABSTRACT Breast cancer is the most common malignancy in women of developed countries. The aim of this study was to investigate whether genistein, a soy phytoestrogen, and 17β‐estradiol (E2) could have effects on the cell cycle and mitochondrial function and dynamics. Three human breast cancer cell lines with different estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) ratio were used: MCF‐7 (high ERα/ERβ ratio), T47D (low ERα/ERβ ratio) and MDA‐MB‐231 (ER‐negative). Cell proliferation, cell cycle, mitochondrial functionality, and mitochondrial dynamics parameters were analyzed. E2 and genistein treatment induced cell proliferation and apoptosis inhibition in MCF‐7, but not in T47D and MDA‐MB‐231. Moreover, genistein treatment produced an up‐regulation of ERβ and a rise in cytochrome c oxidase activity in T47D cells, decreasing the ATP synthase/cytochrome c oxidase ratio. Finally, genistein treatment produced a drop in mitochondrial dynamics only in MCF‐7 cells. In summary, the beneficial effects of genistein consumption depend on the ERα/ERβ ratio in breast cells. Therefore, genistein treatment produces cell cycle arrest and an improvement of mitochondrial functionality in T47D cells with a low ERα/ERβ ratio, but not in MCF‐7 (high ERα/ERβ ratio) and MDA‐MB‐231 (ER‐negative) ones. J. Cell. Biochem. 115: 949–958, 2014. © 2013 Wiley Periodicals, Inc.

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