Abstract
Two recent reports provide compelling insights into the role for RANK and its ligand, RANKL, in progestin-dependent mammary tumorigenesis. These findings build upon a considerable body of evidence pointing to the RANK signaling pathway as being a key mediator of progestin action in the mammary glands.
Highlights
The osteoblast-secreted receptor of activated NF-κB (RANK) ligand (RANKL) activates RANK receptors on osteoclasts to promote their differentiation, maturation and survival, and bone resorption [1]
Whereas RANK is constitutively present within the mammary glands of mice, the local expression of RANK ligand (RANKL) is tightly coordinated with pregnancy-induced expansion of the mammary epithelium during lobulo-alveologenesis [3,4,5]
This RANK- and RANKLmediated development reflects both cell proliferation and survival [3,6,7], which are both processes that are crucial during mammary tumorigenesis
Summary
The osteoblast-secreted receptor of activated NF-κB (RANK) ligand (RANKL) activates RANK receptors on osteoclasts to promote their differentiation, maturation and survival, and bone resorption [1]. Whereas RANK is constitutively present within the mammary glands of mice, the local expression of RANKL is tightly coordinated with pregnancy-induced expansion of the mammary epithelium during lobulo-alveologenesis [3,4,5]. Several of the same hormones that promote this development, including progesterone, prolactin and parathyroid hormone related protein, induce RANKL expression in the mammary glands, in the mammary epithelium [3,4].
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