Journal article
Nutrition and Cancer, 2016
APA
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de la Parra, C., Castillo‐Pichardo, L., Cruz-Collazo, A. M., Cubano, L., Redis, R., Calin, G., & Dharmawardhane, S. (2016). Soy Isoflavone Genistein-Mediated Downregulation of miR-155 Contributes to the Anticancer Effects of Genistein. Nutrition and Cancer.
Chicago/Turabian
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Parra, Columba de la, L. Castillo‐Pichardo, Ailed M Cruz-Collazo, L. Cubano, R. Redis, G. Calin, and S. Dharmawardhane. “Soy Isoflavone Genistein-Mediated Downregulation of MiR-155 Contributes to the Anticancer Effects of Genistein.” Nutrition and Cancer (2016).
MLA
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de la Parra, Columba, et al. “Soy Isoflavone Genistein-Mediated Downregulation of MiR-155 Contributes to the Anticancer Effects of Genistein.” Nutrition and Cancer, 2016.
BibTeX Click to copy
@article{columba2016a,
title = {Soy Isoflavone Genistein-Mediated Downregulation of miR-155 Contributes to the Anticancer Effects of Genistein},
year = {2016},
journal = {Nutrition and Cancer},
author = {de la Parra, Columba and Castillo‐Pichardo, L. and Cruz-Collazo, Ailed M and Cubano, L. and Redis, R. and Calin, G. and Dharmawardhane, S.}
}
ABSTRACT We previously reported that dietary genistein inhibits mammary tumor growth and metastasis of the highly metastatic MDA-MB-435 cancer cells in immunocompromised mice. The purpose herein was to characterize the role of the novel oncogenic microRNA (miRNA) miR-155 in the anticancer effects of genistein in metastatic breast cancer. The effect of genistein was determined on breast cancer cell viability, apoptosis, and expression of miR-155 and its targets. At low physiologically relevant concentrations, genistein inhibits cell viability and induces apoptosis in metastatic MDA-MB-435 and Hs578t breast cancer cells, without affecting the viability of nonmetastatic MCF-7 breast cancer cells. In parallel with reduced cell viability, miR-155 is downregulated, whereas proapoptotic and anticell proliferative miR-155 targets FOXO3, PTEN, casein kinase, and p27 are upregulated in MDA-MB-435 and Hs578t cells in response to genistein treatment. However, miR-155 levels remain unchanged in response to genistein in the MCF-7 cells. Ectopic expression of miR-155 in MDA-MB-435 and Hs578t cells decreases the effects of genistein on cell viability and abrogates the effects of genistein on apoptosis and expression of proapoptotic genes. Therefore, genistein-mediated downregulation of miR-155 contributes to the anticancer effects of genistein in metastatic breast cancer.