Journal
JOURNAL OF MOLECULAR ENDOCRINOLOGY
Volume 48, Issue 1, Pages 61-75Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-11-0078
Keywords
-
Categories
Funding
- NIH [1R15 ES019129-01, 2R15 CA113747-02]
- NSF [0821969]
- American Heart Association [0765160Y]
- Division Of Chemistry
- Direct For Mathematical & Physical Scien [0821969] Funding Source: National Science Foundation
Ask authors/readers for more resources
HOXC10 is a critical player in the development of spinal cord, formation of neurons, and associated with human leukemia. We found that HOXC10 is overexpressed in breast cancer and transcriptionally regulated by estrogen (17 beta-estradiol, E-2). The HOXC10 promoter contains several estrogen response elements (ERE1-7, half-sites). A luciferase-based reporter assay showed that ERE1 and ERE6 of HOXC10 promoter are E-2 responsive. ER alpha and ER beta play critical roles in E-2-mediated activation of HOXC10. Knockdown of ER alpha and ER beta downregulated E-2-induced HOXC10 expression. ER alpha and ER beta bind to ERE1 and ERE6 regions in an E-2-dependent manner. Additionally, knockdown of histone methylases MLL3 and MLL4 (but not MLL1 and MLL2) diminished E-2-induced expression of HOXC10. MLL3 and MLL4 were bound to the ERE1 and ERE6 regions of HOXC10 promoter in an E-2-dependent manner. Overall, we demonstrated that HOXC10 is overexpressed in breast cancer, and it is an E-2-responsive gene. Histone methylases MLL3 and MLL4, along with ERs, regulate HOXC10 gene expression in the presence of E-2. Journal of Molecular Endocrinology (2012) 48, 61-75
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available