AI Article Synopsis
- C/EBPβ is essential for the development of mammary ducts and alveoli in mice, particularly in the presence of progesterone.
- All isoforms of C/EBPβ can activate the progesterone receptor (PR) promoter, with LIP working effectively with c-Jun to boost PR transcription.
- During pregnancy, LIP levels increase, and C/EBPβ and PRB expression patterns suggest that C/EBPβ plays a significant role in promoting PRB expression in the mammary glands.
Article Abstract
CCAAT/enhancer binding protein β (C/EBPβ) is required for murine mammary ductal morphogenesis and alveologenesis. Progesterone is critical for proliferation and alveologenesis in adult mammary glands, and there is a similar requirement for progesterone receptor isoform B (PRB) in alveologenesis. We examined C/EBPβ regulation of PR expression. All three C/EBPβ isoforms, including typically inhibitory LIP, transactivated the PR promoter. LIP, particularly, strongly synergized with c-Jun to drive PR transcription. Endogenous C/EBPβ and c-Jun stimulated a PR promoter-reporter and these two factors showed promoter occupancy on the endogenous PR gene. Additionally, LIP overexpression elevated endogenous PR protein expression. In pregnancy, both PRB and the relative abundance of LIP among C/EBPβ isoforms increase. Consistent with a role in PRB expression, in vivo C/EBPβ and PR isoform A expression showed mutually exclusive localization in mammary epithelium, while C/EBPβ and PRB largely co-localized. We suggest a critical role for C/EBPβ, particularly LIP, in PRB expression.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6153074 | PMC |
| http://dx.doi.org/10.1016/j.mce.2018.06.001 | DOI Listing |
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