Biological characterization of a novel phytoestrogen breviflavone B and investigation of its estrogen receptor-mediated signalling mechanism.
Hormone replacement therapy (HRT) has often been recommended to alleviate menopausal symptoms. Unfortunately, the safety of HRT has been controversial, with numerous studies showing that HRT is associated with increased risk and progression of breast cancer. As such, our study investigated the biol...
Saved in:
Main Author: | |
---|---|
Other Authors: | |
Format: | Final Year Project |
Language: | English |
Published: |
2011
|
Subjects: | |
Online Access: | http://hdl.handle.net/10356/46435 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Institution: | Nanyang Technological University |
Language: | English |
Summary: | Hormone replacement therapy (HRT) has often been recommended to alleviate menopausal symptoms. Unfortunately, the safety of HRT has been controversial, with numerous studies showing that HRT is associated with increased risk and
progression of breast cancer. As such, our study investigated the biological action of
the novel phytoestrogen, breviflavone B (BB), comparing its biological effects with
the endogenous estrogen, 17β-estradiol (E2), so as to gauge the potential of BB for use in hormone replacement therapy. In this study, we demonstrated that BB, like
E2, activates both ERα and ERβ. Paradoxically, despite its ER-agonistic activity, high dose of BB is able to induce apoptosis and inhibit ER-positive breast cancer cell proliferation. This was in contrast to E2, which at high doses, increase ERα-positive breast cancer cell proliferation. There was also a stark difference in the regulation of pS2 and PGR gene expression in presence of high dose of BB compared to E2, which could be a reason for its inhibitory effects on breast cancer cell proliferation. These results from our study suggest that BB may not have the undesirable effects of current HRT in the breast tissue, and thus could be potentially promising as a replacement of estrogen in HRT. |
---|