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 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- People, plus animal or lab work
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- U.S. Department of Defense
- Government
- U.S. Department of Agriculture
- Grants
- U.S. Department of Defense (W81XWH); U.S. Department of Agriculture (6251-5100002-06S)
Based on 2 listed funder(s).
Publication
- Published
- 2012-01-04 · Carcinogenesis · vol. 33 · issue 3 · pp. 652–660
- Publisher
- Oxford University Press
- Cited
- 124 citations · more than 98% of similar papers · 6.4× the field average
- Impact
- Top 10% most cited in its field
- References
- 55 works
- Access
- Free to read
- Research areas
- Cancer Cells and Metastasis · Metastasis and carcinoma case studies
- Keywords
- 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 authors
From US
- Maria Theresa E. MontalesArkansas Children's Nutrition Center
- Omar M. RahalArkansas Children's Nutrition Center; University of Arkansas for Medical Sciences
- Jie KangArkansas Children's Nutrition Center
- Theodore J. RogersArkansas Children's Nutrition Center
- Ronald L. PriorArkansas Children's Nutrition Center
- Xianli WuArkansas Children's Nutrition Center
Abstract
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.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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