期刊
STEM CELL REPORTS
卷 9, 期 4, 页码 1167-1179出版社
CELL PRESS
DOI: 10.1016/j.stemcr.2017.08.011
关键词
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资金
- NIH [R01 CA157675, R01 CA179556]
- NIEHS [T32 ES007015]
- UWCCC Core Grant [NIH P30 CA014520]
- Merial Veterinary Scholars Program grant
- UW Graduate School
- Department of Comparative Biosciences
Hormones drive mammary development and function and play critical roles in breast cancer. Epidemiologic studies link prolactin (PRL) to increased risk for aggressive cancers that express estrogen receptor alpha (ER alpha). However, in contrast to ovarian steroids, PRL actions on the mammary gland outside of pregnancy are poorly understood. We employed the transgenic NRL-PRL model to examine the effects of PRL alone and with defined estrogen/progesterone exposure on stem/progenitor activity and regulatory networks that drive epithelial differentiation. PRL increased progenitors and modulated transcriptional programs, even without ovarian steroids, and with steroids further raised stem cell activity associated with elevated canonical Wnt signaling. However, despite facilitating some steroid actions, PRL opposed steroid-driven luminal maturation and increased CD61(+) luminal cells. Our findings demonstrate that PRL can powerfully influence the epithelial hierarchy alone and temper the actions of ovarian steroids, which may underlie its role in the development of breast cancer.
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