Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/35343
Title: DECIPHERING THE ENHANCEOSOME-MEDIATED TRANSCRIPTIONAL ACTIVATION AND CELL PROLIFERATION IN BREAST CANCER
Authors: KONG SAY LI
Keywords: ERα, FOXA1, GATA3, enhanceosome, cell proliferation, breast cancer
Issue Date: 17-Apr-2012
Source: KONG SAY LI (2012-04-17). DECIPHERING THE ENHANCEOSOME-MEDIATED TRANSCRIPTIONAL ACTIVATION AND CELL PROLIFERATION IN BREAST CANCER. ScholarBank@NUS Repository.
Abstract: Estrogen receptor (ER) is a ligand-inducible hormone nuclear receptor that has important physiology and pathology roles in various human systems. My work focused on understanding the combinatorial complexity of ER, FOXA1 and GATA3 regulatory control on a genomic scale. We observe that these three transcription factors (TFs) form a functional enhanceosome that regulates the genes driving core ER function and cooperatively modulate the transcriptional networks previously ascribed to ER alone. We demonstrate that these enhanceosome occupied sites are associated with optimal enhancer characteristics with highest p300 coactivator recruitment, RNA Pol II occupancy, and chromatin opening. Most importantly, we show that the transfection of all three TFs was necessary to reprogramme the ER-negative cells to restore the estrogen responsive growth resembling estrogen treated ER-positive cells. Cumulatively, these results suggest that all the enhanceosome components comprising ER, FOXA1 and GATA3 are necessary for the full repertoire of cancer associated effects of the ER.
URI: http://scholarbank.nus.edu.sg/handle/10635/35343
Appears in Collections:Ph.D Theses (Open)

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Kong SL thesis.pdf3.49 MBAdobe PDF

OPEN

NoneView/Download

Page view(s)

175
checked on Dec 11, 2017

Download(s)

31
checked on Dec 11, 2017

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.