No wonder b.c. incident increases up to 4 years after pregnancy...
Pin1 in breast development
The mammary gland undergoes a sequence of dynamic changes throughout the female life cycle, especially during
pregnancy. These developmental changes depend on the responsiveness of the mammary epithelial cells to hormones and growth factors and on the activation of various intracellular signaling pathways [
51-
53].
We observed that
Pin1 knockout mice display a developmental defect during
pregnancy in preparation for lactation [
37]. Before
pregnancy, the mammary epithelial ducts from both wild-type and
Pin1-/- female mice develop normally. These results indicate that
Pin1 is not required for the development of the primary mammary tree, but rather is required for the rapid and timely expansion of mammary epithelial compartment in preparation for lactation. During
pregnancy, the mammary epithelial ducts rapidly extend their side branches and build up alveoli, which replace the mammary fat pad and form lobules in preparation for lactation.
Pin1-/- female mice, however, show severely reduced mammary epithelial duct development during
pregnancy, and the mammary gland fails to undergo the usual massive expansion [
37]. This phenotype in the
Pin1 knockout mouse is strongly reminiscent of the phenotype resulting from the deletion of cyclin D1, which has a well-established role in the development of breast epithelial cells [
54,
55]. Consistently, protein levels of cyclin D1 are decreased in mammary epithelial cells of
Pin1 knock-out mice [
37]. These results indicate that
Pin1 plays an important role in breast development, probably via regulation of cyclin D1 function. This conclusion has been independently supported by various studies linking
Pin1 to cyclin D1 and breast cancer, as described below.
COMPLETE ARTICLE AT LINK BELOW.
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PS RHONDA, REMEMBER WHEN YOU POSTED THAT SICHUAN PEPPER CAN INHIBIT CYLCIN D TO HELP STOP PROLIFERATION OF BREAST CELLS AND BREAST CANCER? AS YOU CAN SEE ABOVE, CYCLIN D IS A BAD THING TO HAVE AND IS CAUSED BY INCREASED PIN1.