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Department of Molecular Biology, Institute of Basic Medicine, Chinese PLA General Hospital, 28 Fu Xing Road, Beijing 100853, China
1 Department of Endocrinology, Chinese PLA General Hospital, 28 Fu Xing Road, Beijing 100853, China
2 Department of Hematology, Chinese PLA General Hospital, 28 Fu Xing Road, Beijing 100853, China
(Requests for offprints should be addressed to Y-M Mu; Email: muyiming{at}301hospital.com.cn)
* (Y-L Zhao and W-D Han contributed equally to this work)
LRP16 gene expression is induced by 17-ßestradiol (E2) via estrogen receptor alpha (ER
) in MCF-7 human breast cancer cells. A previous study also demonstrated that ectopic expression of LRP16 gene promoted MCF-7 cell proliferation. To explore the mechanism of hormone-induced LRP16 gene expression, the LRP16 gene promoter region (–2600 to –24 bp upstream of the LRP16 gene translation starting site) was analyzed in the present study by using different 5'-truncated constructs, and a luciferase reporter. The 5'-flanking sequence of –676 to –24 bp (pGL3-S5) was found to be E2-responsive. After exchange of the fragment from –213 to –24 bp with the TK gene proximal promoter region in pGL3-S5, E2 still induced reporter gene activity in MCF-7 and HeLa cells. Sequence analysis showed that the pGL3-S6 (–676 to –214) sequence contains two motifs that may contribute to E2-induced transactivation; namely, an estrogen-responsive element (ERE) half-site/Sp1 at –246 to –227 bp and an E-box site at –225 to –219 bp. Further deletion and mutation analysis of these two motifs indicated that both the 1/2 ERE and Sp1 binding sites were required for E2 action, while E-box deletion did not affect the luciferase activity in MCF-7 and HeLa cells. The results of gel mobility shift and chromatin immunoprecipitation assays confirmed that both ERand Sp1 were required for hormone-induced transactivation, which involved both ERand Sp1 directly binding to DNA. Taken together, these findings suggest that ERand Sp1 play a role in activation of the human LRP16 gene promoter.
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