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Genistein Modulates Proliferation and Mitochondrial Functionality in Breast Cancer Cells Depending on ERalpha/ERbeta Ratio
Journal of cellular biochemistry, 2014-05, Vol.115 (5), p.949-958
Pons, Daniel Gabriel
Nadal-Serrano, Mercedes
Blanquer-Rossello, M. Mar
Sastre-Serra, Jorge
Oliver, Jordi
Roca, Pilar
2014
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Pons, Daniel Gabriel
Nadal-Serrano, Mercedes
Blanquer-Rossello, M. Mar
Sastre-Serra, Jorge
Oliver, Jordi
Roca, Pilar
Titel
Genistein Modulates Proliferation and Mitochondrial Functionality in Breast Cancer Cells Depending on ERalpha/ERbeta Ratio
Ist Teil von
Journal of cellular biochemistry, 2014-05, Vol.115 (5), p.949-958
Ort / Verlag
United States: Blackwell Publishing Ltd
Erscheinungsjahr
2014
Quelle
MEDLINE
Beschreibungen/Notizen
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.
Sprache
Englisch
Identifikatoren
ISSN: 0730-2312
eISSN: 1097-4644
DOI: 10.1002/jcb.24737
Titel-ID: cdi_proquest_miscellaneous_1504455742
Format
–
Schlagworte
17β-ESTRADIOL
,
APOPTOSIS
,
ATP
,
ATP synthase
,
Breast cancer
,
Breast Neoplasms - genetics
,
Breast Neoplasms - pathology
,
Cancer
,
CELL CYCLE
,
Cell growth
,
CELL PROLIFERATION
,
Cell Proliferation - drug effects
,
Cytochrome
,
Cytochrome-c oxidase
,
Cytochromes
,
Developed countries
,
Estradiol - metabolism
,
Estrogen Receptor alpha - metabolism
,
Estrogen Receptor beta - metabolism
,
ESTROGEN RECEPTORS
,
Estrogens
,
Female
,
Gene Expression Regulation, Neoplastic - drug effects
,
GENISTEIN
,
Genistein - administration & dosage
,
Humans
,
Malignancy
,
MCF-7 Cells
,
MITOCHONDRIA
,
Mitochondria - drug effects
,
Mitochondria - metabolism
,
Oestrogens
,
Oxidase
,
Phytoestrogens
,
Proliferation
,
Receptors
,
Sex hormones
,
Tumor cell lines
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