Multiple data suggest a relationship between thyroid hormone (triiodothyronine (T3)) and carcinogenesis. Studies on breast cancer have been inconclusive, suggesting contradictory effects of thyroid status and diseases. Recently, we reported that expression of the extracellular matrix glycoprotein te
Lactogenic hormones and Tenascin-C regulate C/EBPα and β in mammary epithelial cells
✍ Scribed by Nathalie Cella; Ruth Chiquet-Ehrismann; Nancy E. Hynes
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 223 KB
- Volume
- 76
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
✦ Synopsis
Mammary epithelial cell differentiation depends on lactogenic hormones, growth factors, and cell-cell and cell-substrate interactions, all of which modulate transcription factors essential for milk protein gene expression. The CCAAT/enhancer binding protein (C/EBP) family and the signal transducer and activator of transcription 5 (Stat5) have been implicated in mammary epithelial cell growth and differentiation. We have investigated the effects of extracellular matrix components and lactogenic hormones on C/EBP and Stat5 activity. In the mammary gland, tenascin is expressed mainly during embryogenesis and carcinogenesis and in cell culture tenascin downregulates -casein gene expression. In HC11 mammary cells, we found that tenascin, but not laminin or fibronectin, specifically downregulated C/EBP␣ levels but had no effect on Stat5 amount or DNA binding activity. Furthermore, we found that the lactogenic hormones, glucocorticoids, prolactin, and insulin, had no effect on C/EBP␣ and C/EBP protein levels but downregulated the DNA binding activity of the transcriptional repressor C/EBPLIP. Thus, C/EBP␣ and  are regulated by tenascin and lactogenic hormones in mammary epithelial cells.
📜 SIMILAR VOLUMES
## Abstract CCAAT/Enhancer binding proteins (C/EBPs) play important roles in the regulation of cell growth and differentiation. This study investigated the expression and function of C/EBPβ isoforms in the mouse mammary gland, mammary tumors, and a nontransformed mouse mammary epithelial cell line
## Abstract Molecular‐targeted therapy is a hopeful approach for pancreatic cancer. Silencing of tumor suppressor genes can occur by histone deacetylation and/or DNA methylation in the promoter. Here, we identified epigenetically silenced genes in pancreatic cancer cells. Pancreatic cancer cell lin
## Abstract “Loss of function” alterations in growth inhibitory signal transduction pathways are common in cancer cells. In this study, we show that growth arrest (GA) treatments—serum and growth factor withdrawal and growth inhibitory IL‐6 family cytokines (Interleukin‐6 and Oncostatin M (OSM))—in
## Abstract CCAAT/enhancer binding protein δ (C/EBPδ) plays a key role in mammary epithelial cell G~0~ growth arrest. C/EBPδ gene expression is down‐regulated in rodent mammary tumorigenesis and in human breast cancer, suggesting that “loss of function” alterations in C/EBPδ gene expression are com
## Abstract Previous studies have shown that both the signal transducer and activator of transcription 5 (STAT5) and the CCAAT enhancer binding proteins (C/EBPs) are involved in the regulation of casein gene expression by mammary epithelial cells. Prolactin (Prl) activation of STAT5 is necessary fo