Document Type
Article
Publication Date
2-1-2011
Publication Title
The Journal of Steroid Biochemistry and Molecular Biology
Abstract
It has been demonstrated that growth factors produced by breast cancer cells stimulate aromatase expression in both breast cancer and adjacent adipose fibroblasts and stromal cells. However, whether these growth factors affect aromatase activity by other mechanisms still remain unclear. In the current study, MCF-7aro and T47Daro aromatase transfected breast carcinoma cells were used to explore the mechanisms of post-transcriptional regulation of aromatase activity by growth factor pathways. Our study reveals that PI3K/Akt and MAPK inhibitors suppressed aromatase activity in MCF-7aro cells. However, PI3K/Akt pathway inhibitors stimulated aromatase activity in T47Daro cells. This is due to enhanced MAPK phosphorylation as compensation after the PI3K/Akt pathway has been blocked. IGF-1 treatment increased aromatase activity in both breast cancer cell lines. In addition, LTEDaro cells (long-term estrogen deprived MCF-7aro cells) which have enhanced MAPK activity, show higher aromatase activity compared to parental MCF-7aro cells, but the aromatase protein level remains the same. These results suggest that aromatase activity could be enhanced by growth factor signaling pathways via post-transcriptional mechanisms.
Recommended Citation
Su, Bin; Wong, Cynthie; Hong, Yanyan; and Chen, Shiuan, "Growth Factor Signaling Enhances Aromatase Activity of Breast Cancer Cells Via Post-Transcriptional Mechanisms" (2011). Chemistry Faculty Publications. 390.
https://engagedscholarship.csuohio.edu/scichem_facpub/390
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
DOI
10.1016/j.jsbmb.2010.11.012
Version
Postprint
Volume
123
Issue
2017-03-05
Comments
This work was supported by grants from the National Institutes of HealthCA44735 (SC), ES08528 (SC), and a startup fund from CSU (BSu).