Abstract
The diversity of membrane-initiated progesterone actions has made characterization and establishment of its biological importance a complicated endeavor. A new study by Zuo and colleagues shows that progesterone via endogenous membrane progesterone receptor-α acts as a negative regulator of proliferation and epithelial to mesenchymal transition in a breast cancer cell line. These progesterone-mediated actions appear to be regulated through epidermal growth factor receptor and phosphatidylinositol 3-kinase signaling localized in caveolae. Moreover, the study shows expression of membrane progesterone receptor-α in benign and malignant breast cancer tissues. These data bring forth novel concepts with regard to progesterone actions in the breast; however, further work is warranted to fully characterize the physiologic actions of extra-nuclear progesterone signaling in the breast.
Highlights
The diversity of membrane-initiated progesterone actions has made characterization and establishment of its biological importance a complicated endeavor
The perception has been that the physiological actions of progesterone are mediated via nuclear progesterone receptors (PRs) that act as transcription factors to alter gene expression [2]
It has been shown that in breast cancer cells the classical PRB directly interacts with Src to mediate progesterone-triggered Src and downstream mitogen-activated protein kinase (MAPK) activation [6]
Summary
The diversity of membrane-initiated progesterone actions has made characterization and establishment of its biological importance a complicated endeavor. The perception has been that the physiological actions of progesterone are mediated via nuclear progesterone receptors (PRs) that act as transcription factors to alter gene expression [2]. Substantial evidence implicates membrane- or cytoplasmic-localized classical steroid receptors as regulators of non-genomic steroid signaling, and progesterone is no exception [3].
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