Título:
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ApoA-I Mimetic administration, but not increased apoA-I-containing HDL, inhibits tumour growth in a mouse model of inherited breast cancer.
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Autor/a:
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Cedó Giné, Lídia; García León, Annabel; Baila Rueda, Lucía; Santos, David; Grijalva, Victor; Martínez Cignoni, Melanie Raquel; Carbo Marques, Jose Maria; Metso, Jari; López Vilaró, Laura; Zorzano Olarte, Antonio; Valledor Fernández, Annabel; Cenarro, Ana; Jauhiainen, Matti; Lerma, Enrique; Fogelman, Alan M.; Reddy, Srinivasa T.; Escolà i Gil, Joan Carles; Blanco-Vaca, Francisco
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Otros autores:
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Universitat de Barcelona |
Abstract:
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Low levels of high-density lipoprotein cholesterol (HDLc) have been associated with breast cancer risk, but several epidemiologic studies have reported contradictory results with regard to the relationship between apolipoprotein (apo) A-I and breast cancer. We aimed to determine the effects of human apoA-I overexpression and administration of specific apoA-I mimetic peptide (D-4F) on tumour progression by using mammary tumour virus-polyoma middle T-antigen transgenic (PyMT) mice as a model of inherited breast cancer. Expression of human apoA-I in the mice did not affect tumour onset and growth in PyMT transgenic mice, despite an increase in the HDLc level. In contrast, D-4F treatment significantly increased tumour latency and inhibited the development of tumours. The effects of D-4F on tumour development were independent of 27-hydroxycholesterol. However, D-4F treatment reduced the plasma oxidized low-density lipoprotein (oxLDL) levels in mice and prevented oxLDL-mediated proliferative response in human breast adenocarcinoma MCF-7 cells. In conclusion, our study shows that D-4F, but not apoA-I-containing HDL, hinders tumour growth in mice with inherited breast cancer in association with a higher protection against LDL oxidative modification |
Materia(s):
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-Càncer de mama -Hiperlipoproteïnes -Ratolins transgènics -Pèptids -Breast cancer -High density lipoproteins -Transgenic mice -Peptides |
Derechos:
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cc-by (c) Cedó et al., 2016
http://creativecommons.org/licenses/by/3.0/es |
Tipo de documento:
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Artículo Artículo - Versión publicada |
Editor:
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Nature Publishing Group
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