Estrogen induced beta-1,4-galactosyltransferase 1 expression regulates proliferation of human breast cancer MCF-7 cells
- Authors
- Choi, HJ[Choi, Hee-Jung]; Chung, TW[Chung, Tae-Wook]; Kim, CH[Kim, Cheorl-Ho]; Jeong, HS[Jeong, Han-Sol]; Joo, M[Joo, Myungsoo]; Youn, B[Youn, BuHyun]; Ha, KT[Ha, Ki-Tae]
- Issue Date
- 5-Oct-2012
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Beta 1,4-galactosyltransferase 1; Estrogen; Breast
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.426, no.4, pp.620 - 625
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 426
- Number
- 4
- Start Page
- 620
- End Page
- 625
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/63927
- DOI
- 10.1016/j.bbrc.2012.08.140
- ISSN
- 0006-291X
- Abstract
- Beta 1,4-galactosyltransferase 1 (B4GALT1) synthesizes galactose beta-1,4-N-acetylglucosamine (Gal beta 1-4GlcNAc) groups on N-linked sugar chains of glycoproteins, which play important roles in many biological events, including the proliferation and migration of cancer cells. A previous microarray study reported that this gene is expressed by estrogen treatment in breast cancer. In this study, we examined the regulatory mechanisms and biological functions of estrogen-induced B4GALT1 expression. Our data showed that estrogen-induced expression of B4GALT1 is localized in intracellular compartments and in the plasma membrane. In addition, B4GALT1 has an enzyme activity involved in the production of the Gal beta 1-4GlcNAc structure. The result from a promoter assay and chromatin immunoprecipitation revealed that 3 different estrogen response elements (EREs) in the B4GALT1 promoter are critical for responsiveness to estrogen. In addition, the estrogen antagonists ICI 182,780 and ER-alpha-ERE binding blocker TPBM inhibit the expression of estrogen-induced B4GALT1. However, the inhibition of signal molecules relating to the extra-nuclear pathway, including the G-protein coupled receptors. Ras, and mitogen-activated protein kinases, had no inhibitory effects on B4GALT1 expression. The knock-down of the B4GALT1 gene and the inhibition of membrane B4GALT1 function resulted in the significant inhibition of estrogen-induced proliferation of MCF-7 cells. Considering these results, we propose that estrogen regulates the expression of B4GALT1 through the direct binding of ER-alpha to ERE and that the expressed B4GALT1 plays a crucial role in the proliferation of MCF-7 cells through its activity as a membrane receptor. (C) 2012 Elsevier Inc. All rights reserved.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Science > Department of Biological Science > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/63927)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.