genotoxic exposure during juvenile growth of mammary gland depletes stem cell activity and inhibits wnt signaling不会暴露在少年乳腺干细胞活动消耗的增长和抑制wnt信号.pdfVIP
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genotoxic exposure during juvenile growth of mammary gland depletes stem cell activity and inhibits wnt signaling不会暴露在少年乳腺干细胞活动消耗的增长和抑制wnt信号
Genotoxic Exposure during Juvenile Growth of
Mammary Gland Depletes Stem Cell Activity and Inhibits
Wnt Signaling
Kristine S. Klos, Soyoung Kim, Caroline M. Alexander*
McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States of America
Abstract
Various types of somatic stem cell have been tested for their response to genotoxic exposure, since these cells are likely to
be important to regeneration, aging and cancer. In this study, we evaluated the response of mammary stem cells to
genotoxic exposure during ductal growth in juveniles. Exposure to the polycyclic aromatic hydrocarbon (DMBA; 7,12
dimethylbenz[a]anthracene) had no gross effect on outgrowth and morphogenesis of the ductal tree, or upon
lobuloalveolar growth during pregnancy. However, by fat pad assay, we found that mammary stem cell activity was reduced
by 80% in glands from adults that were exposed to genotoxins as juveniles. The associated basal cell lineage was depleted.
Both basal and luminal cells showed a robust response to genotoxic exposure (including cH2AX phosphorylation, pS15p53
and pT68Chk2), with durable hyperproliferation, but little cytotoxicity. Since the phenotype of these glands (low basal cell
fraction, low stem cell activity) phenocopies mammary glands with loss of function for Wnt signaling, we measured Wnt
signaling in genotoxin-exposed glands, and found a durable reduction in the activation of the canonical signaling Wnt
receptors, Lrp5/6. Furthermore, when mammary epithelial cells were treated with Wnt3a, DMBA exposure reduced the basal
cell population and Lrp activation was ablated. We conclude that during active ductal growth, Wnt-dependent mammary
stem cells are sensitized to cell death by genotoxin exposure. Our conclusion
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