Research Papers:
CtBP1 associates metabolic syndrome and breast carcinogenesis targeting multiple miRNAs
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Abstract
Paola De Luca1, Guillermo N. Dalton1, Georgina D. Scalise1, Cristian P. Moiola1, Juliana Porretti1, Cintia Massillo1, Edith Kordon2, Kevin Gardner3, Florencia Zalazar1, Carolina Flumian4, Laura Todaro4, Elba S. Vazquez5, Roberto Meiss6, Adriana De Siervi1
1Laboratorio de Oncología Molecular y Nuevos Blancos Terapéuticos, Instituto de Biología y Medicina Experimental (IBYME), CONICET, Buenos Aires, Argentina
2Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), and Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), CONICET, Buenos Aires, Argentina
3National Cancer Institute and National Institute of Minority Health and Disparities, National Institutes of Health, Bethesda, MD, USA
4Área de Investigación del Instituto de Oncología A.H. Roffo, Universidad de Buenos Aires, Buenos Aires, Argentina
5Laboratorio de Inflamación y Cáncer, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales (FCEN), Universidad de Buenos Aires (UBA), IQUIBICEN – CONICET, Buenos Aires, Argentina
6Departamento de Patología, Instituto de Estudios Oncológicos, Academia Nacional de Medicina, Buenos Aires, Argentina
Correspondence to:
Adriana De Siervi, email: [email protected]
Keywords: CtBP1, metabolic syndrome, high fat diet, breast cancer, miRNAs
Received: December 22, 2015 Accepted: February 11, 2016 Published: February 25, 2016
ABSTRACT
Metabolic syndrome (MeS) has been identified as a risk factor for breast cancer. C-terminal binding protein 1 (CtBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio. High fat diet (HFD) increases intracellular NADH. We investigated the effect of CtBP1 hyperactivation by HFD intake on mouse breast carcinogenesis. We generated a MeS-like disease in female mice by chronically feeding animals with HFD. MeS increased postnatal mammary gland development and generated prominent duct patterns with markedly increased CtBP1 and Cyclin D1 expression. CtBP1 induced breast cancer cells proliferation. Serum from animals with MeS enriched the stem-like/progenitor cell population from breast cancer cells. CtBP1 increased breast tumor growth in MeS mice modulating multiple genes and miRNA expression implicated in cell proliferation, progenitor cells phenotype, epithelial to mesenchymal transition, mammary development and cell communication in the xenografts. These results define a novel function for CtBP1 in breast carcinogenesis.
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