Heather M Brechbuhl and Carol A Sartorius
Endocrinology, Volume 165, Issue 10, October 2024, bqae109
https://doi.org/10.1210/endocr/bqae109
Progesterone receptors (PRs) are routinely measured alongside estrogen receptors (ERs) following breast cancer diagnoses as predictive markers of response to endocrine therapies, partly because of PR’s status as an estrogen-responsive gene. Beyond its biomarker status, the role of PR in breast tumorigenesis, growth, and progression remains contentious. Whether PR exerts pro- or anti-tumorigenic signals depends on several factors, including the type of ligand used (progesterone or synthetic analogs), the relative abundance of the 2 naturally occurring PR isoforms (PR-A and PR-B), and its interplay with ER. One of the most consistently described functions of PR is regulation of breast cancer stem cells (CSCs) (1), reflecting its pivotal role in controlling mammary stem cells in normal breast tissue. The impact of PR regulation of CSCs remains unclear, partially because of oversimplified model systems used in these studies. A confounding factor is that most studies on PR action have been tumor cell-centric, lacking consideration of cancer cell interactions with the tumor microenvironment.
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