Repression of mammosphere formation of human breast cancer cells by soy isoflavone genistein and blueberry polyphenolic acids suggests diet-mediated targeting of cancer stem-like/progenitor cells
Montales MT, Rahal OM, Kang J, Rogers TJ, Prior RL, Wu X, Simmen RC
Carcinogenesis · 86 citas
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Cómo se estudió
- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas, más trabajo en animales o laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- U.S. Department of Defense
- Gobierno
- U.S. Department of Agriculture
- Subvenciones
- U.S. Department of Defense (W81XWH); U.S. Department of Agriculture (6251-5100002-06S)
Según 2 financiadores declarados.
Publicación
- Publicado
- 2012-01-04 · Carcinogenesis · vol. 33 · número 3 · págs. 652–660
- Editorial
- Oxford University Press
- Citado
- 124 citas · más que el 98% de estudios similares · 6.4× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 55 trabajos
- Acceso
- Lectura gratuita
- Áreas de investigación
- Cancer Cells and Metastasis · Metastasis and carcinoma case studies
- Palabras clave
- Stem cell, Progenitor cell, CD44, Biology, Cancer research, Cancer stem cell, PTEN, CD24, Estrogen receptor, Genistein, Wnt signaling pathway, Cell biology, Endocrinology, Cancer, PI3K/AKT/mTOR pathway, Cell, Breast cancer, Signal transduction, Biochemistry, Genetics
- MeSH
- cell line, tumor, animals, humans, mice, breast neoplasms, mammary neoplasms, experimental, phosphorylcholine, isoflavones, genistein, soybean proteins, plant extracts, female, pten phosphohydrolase, neoplastic stem cells, polyphenols, blueberry plants, hyaluronan receptors, cd24 antigen
7 autores
- Maria Theresa E. Montales🇺🇸Arkansas Children's Nutrition Center
- Omar M. Rahal🇺🇸Arkansas Children's Nutrition Center; University of Arkansas for Medical Sciences
- Jie Kang🇺🇸Arkansas Children's Nutrition Center
- Theodore J. Rogers🇺🇸Arkansas Children's Nutrition Center
- Ronald L. Prior🇺🇸Arkansas Children's Nutrition Center
- Xianli Wu🇺🇸Arkansas Children's Nutrition Center
- Rosalia C. M. Simmen🇺🇸 · autor de correspondenciaArkansas Children's Nutrition Center; University of Arkansas for Medical Sciences
Resumen
El texto original del estudio, en el idioma en que se publicó.
Mammary stem cells are undifferentiated epithelial cells, which initiate mammary tumors and render them resistant to anticancer therapies, when deregulated. Diets rich in fruits and vegetables are implicated in breast cancer risk reduction, yet underlying mechanisms are poorly understood. Here, we addressed whether dietary factors selectively target mammary epithelial cells that display stem-like/progenitor subpopulations with previously recognized tumor-initiating potential. Using estrogen receptor-positive MCF-7 and estrogen receptor-negative MDA-MB-231 human breast cancer cell lines and freshly isolated epithelial cells from MMTV-Wnt-1 transgenic mouse mammary tumors, we demonstrate that sera of adult mice consuming soy isoflavone genistein (GEN) or blueberry (BB) polyphenol-containing diets alter the population of stem-like/progenitor cells, as measured by their functional ability to self-renew and form anchorage-independent spheroid cultures in vitro at low frequency (1-2%). Serum effects on mammosphere formation were dose-dependently replicated by GEN (40 nM >2 μM) and targeted the basal stem-like CD44+/CD24-/ESA+ and the luminal progenitor CD24+ subpopulations in MDA-MB-231 and MCF-7 cells. GEN inhibition of mammosphere formation was mimicked by the Akt inhibitor perifosine and was associated with enhanced tumor suppressor phosphatase and tensin homologue deleted on chromosome ten (PTEN) expression. In contrast, a selected mixture of BB phenolic acids was only active in MDA-MD-231 cells and its CD44+/CD24-/ESA+ subpopulation, and this activity was independent of induction of PTEN expression. These findings delineate a novel and selective function of distinct dietary factors in targeting stem/progenitor cell populations in estrogen receptor-dependent and -independent breast cancers.
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