PMID- 24992181
OWN - NLM
STAT- MEDLINE
DCOM- 20150330
LR  - 20211021
IS  - 1944-9917 (Electronic)
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 28
IP  - 8
DP  - 2014 Aug
TI  - ERbeta- and prostaglandin E2-regulated pathways integrate cell proliferation via 
      Ras-like and estrogen-regulated growth inhibitor in endometriosis.
PG  - 1304-15
LID - 10.1210/me.2013-1421 [doi]
AB  - In endometriosis, stromal and epithelial cells from the endometrium form 
      extrauterine lesions and persist in response to estrogen (E2) and prostaglandin 
      E2 (PGE2). Stromal cells produce excessive quantities of estrogen and PGE2 in a 
      feed-forward manner. However, it is unknown how estrogen stimulates cell 
      proliferation and survival for the establishment and persistence of disease. 
      Previous studies suggest that estrogen receptor-beta (ERbeta) is strikingly 
      overexpressed in endometriotic stromal cells. Thus, we integrated genome-wide ERbeta 
      binding data from previously published studies in breast cells and gene 
      expression profiles in human endometriosis and endometrial tissues (total sample 
      number = 81) and identified Ras-like, estrogen-regulated, growth inhibitor (RERG) 
      as an ERbeta target. Estradiol potently induced RERG mRNA and protein levels in 
      primary endometriotic stromal cells. Chromatin immunoprecipitation demonstrated 
      E2-induced enrichment of ERbeta at the RERG promoter region. PGE2 via protein kinase 
      A phosphorylated RERG and enhanced the nuclear translocation of RERG. RERG 
      induced the proliferation of primary endometriotic cells. Overall, we 
      demonstrated that E2/ERbeta and PGE2 integrate at RERG, leading to increased 
      endometriotic cell proliferation and represents a novel candidate for therapeutic 
      intervention.
FAU - Monsivais, D
AU  - Monsivais D
AD  - Division of Reproductive Biology Research (D.M., M.T.D., P.Y., J.S.C., A.N., 
      S.S.M., M.O., C.M.E., M.E.P., E.S., S.E.B.), Department of Obstetrics and 
      Gynecology, Feinberg School of Medicine, Northwestern University, Northwestern 
      University Biomedical Informatics Center (part of the Northwestern CTSA) and The 
      Robert H. Lurie Comprehensive Cancer Center (G.F.), and Department of Pathology 
      (J.J.W.), Feinberg School of Medicine, Northwestern University, Chicago, Illinois 
      60611.
FAU - Dyson, M T
AU  - Dyson MT
FAU - Yin, P
AU  - Yin P
FAU - Coon, J S
AU  - Coon JS
FAU - Navarro, A
AU  - Navarro A
FAU - Feng, G
AU  - Feng G
FAU - Malpani, S S
AU  - Malpani SS
FAU - Ono, M
AU  - Ono M
FAU - Ercan, C M
AU  - Ercan CM
FAU - Wei, J J
AU  - Wei JJ
FAU - Pavone, M E
AU  - Pavone ME
FAU - Su, E
AU  - Su E
FAU - Bulun, S E
AU  - Bulun SE
LA  - eng
GR  - R25 GM079300/GM/NIGMS NIH HHS/United States
GR  - R37 HD038691/HD/NICHD NIH HHS/United States
GR  - T32 DK007169/DK/NIDDK NIH HHS/United States
GR  - R37HD038691/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20140703
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (Estrogen Receptor beta)
RN  - 4TI98Z838E (Estradiol)
RN  - EC 3.6.1.- (GTP Phosphohydrolases)
RN  - EC 3.6.1.-. (RERG protein, human)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Adult
MH  - Cell Nucleus/metabolism
MH  - *Cell Proliferation
MH  - Dinoprostone/*physiology
MH  - Endometriosis/*metabolism/pathology
MH  - Estradiol/physiology
MH  - Estrogen Receptor beta/*physiology
MH  - Female
MH  - GTP Phosphohydrolases/*metabolism
MH  - Gene Expression Regulation
MH  - HEK293 Cells
MH  - Humans
MH  - Protein Transport
PMC - PMC4116594
EDAT- 2014/07/06 06:00
MHDA- 2015/03/31 06:00
PMCR- 2015/08/01
CRDT- 2014/07/04 06:00
PHST- 2014/07/04 06:00 [entrez]
PHST- 2014/07/06 06:00 [pubmed]
PHST- 2015/03/31 06:00 [medline]
PHST- 2015/08/01 00:00 [pmc-release]
AID - ME-13-1421 [pii]
AID - 10.1210/me.2013-1421 [doi]
PST - ppublish
SO  - Mol Endocrinol. 2014 Aug;28(8):1304-15. doi: 10.1210/me.2013-1421. Epub 2014 Jul 
      3.