PMID- 19847644
OWN - NLM
STAT- MEDLINE
DCOM- 20100927
LR  - 20191210
IS  - 1573-7217 (Electronic)
IS  - 0167-6806 (Linking)
VI  - 122
IP  - 2
DP  - 2010 Jul
TI  - Menin, a product of the MENI gene, binds to estrogen receptor to enhance its 
      activity in breast cancer cells: possibility of a novel predictive factor for 
      tamoxifen resistance.
PG  - 395-407
LID - 10.1007/s10549-009-0581-0 [doi]
AB  - Multiple coactivator and corepressor complexes play an important role in 
      endocrine processes and breast cancer; in particular, estrogen and estrogen 
      receptor-alpha (ERalpha) promote the proliferation of breast cancer cells. Menin 
      is a tumor suppressor encoded by Men1 that is mutated in the human-inherited 
      tumor syndrome multiple endocrine neoplasia type 1 (MEN1); it also serves as a 
      critical link in the recruitment of nuclear receptor-mediated transcription. 
      Here, we show that menin expressed in breast cancer cell line MCF-7 is 
      colocalized with ERalpha and functions as a direct coactivator of ER-mediated 
      transcription in breast cancer cells. In MCF-7 cells, coexpression of menin and 
      estrogen-response element-luciferase induced the activity of the latter in a 
      hormone-dependent manner. Cells knocked down for ERalpha exhibited impaired 
      ERE-luciferase activity induced by menin. Mammalian two-hybrid assay and GST 
      pull-down assays indicated that menin could interact with the AF-2 domain of 
      ERalpha. These results indicate that menin is a direct activator of ERalpha 
      function. Tamoxifen inhibited the binding of menin to AF-2 in mammalian 
      two-hybrid assay, but in menin-overexpressing clones, tamoxifen suppressed 
      ERE-luciferase activity only to the levels of nontreated wild-type MCF-7. In a 
      clinical study with 65 ER-positive breast cancer samples-all of which had been 
      treated with tamoxifen for 2-5 years as adjuvant therapies--menin-positive tumors 
      had a worse outcome than menin-negative ones. These indicated that menin can 
      function as a transcriptional regulator of ERalpha and is a possible predictive 
      factor for tamoxifen resistance.
FAU - Imachi, Hitomi
AU  - Imachi H
AD  - Division of Endocrinology and Metabolism, Department of Internal Medicine, 
      Faculty of Medicine, Kagawa University, 1750-1 Ikenobe Miki-cho, Kita-gun, 
      Kagawa, Japan.
FAU - Murao, Koji
AU  - Murao K
FAU - Dobashi, Hiroaki
AU  - Dobashi H
FAU - Bhuyan, Mohammad M
AU  - Bhuyan MM
FAU - Cao, Xueyuan
AU  - Cao X
FAU - Kontani, Keiichi
AU  - Kontani K
FAU - Niki, Shoko
AU  - Niki S
FAU - Murazawa, Chisa
AU  - Murazawa C
FAU - Nakajima, Hiroo
AU  - Nakajima H
FAU - Kohno, Norio
AU  - Kohno N
FAU - Yamashita, Hiroko
AU  - Yamashita H
FAU - Iwase, Hirotaka
AU  - Iwase H
FAU - Hayashi, Shin-ichi
AU  - Hayashi S
FAU - Ishida, Toshihiko
AU  - Ishida T
FAU - Yamauchi, Akira
AU  - Yamauchi A
LA  - eng
PT  - Journal Article
DEP - 20091022
PL  - Netherlands
TA  - Breast Cancer Res Treat
JT  - Breast cancer research and treatment
JID - 8111104
RN  - 0 (Estrogen Antagonists)
RN  - 0 (Estrogen Receptor alpha)
RN  - 0 (MEN1 protein, human)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 094ZI81Y45 (Tamoxifen)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
MH  - Animals
MH  - Binding Sites
MH  - Breast Neoplasms/drug therapy/genetics/*metabolism/mortality/pathology
MH  - COS Cells
MH  - Cell Line, Tumor
MH  - Chemotherapy, Adjuvant
MH  - Chlorocebus aethiops
MH  - Disease-Free Survival
MH  - *Drug Resistance, Neoplasm
MH  - Estradiol/*metabolism
MH  - Estrogen Antagonists/*therapeutic use
MH  - Estrogen Receptor alpha/antagonists & inhibitors/genetics/*metabolism
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Kaplan-Meier Estimate
MH  - Middle Aged
MH  - Neoplasm Staging
MH  - Nuclear Proteins/metabolism
MH  - Prognosis
MH  - Promoter Regions, Genetic
MH  - Protein Interaction Mapping
MH  - Proto-Oncogene Proteins/genetics/*metabolism
MH  - RNA Interference
MH  - Recombinant Fusion Proteins/metabolism
MH  - Tamoxifen/*therapeutic use
MH  - Time Factors
MH  - Transcriptional Activation
MH  - Transfection
MH  - Two-Hybrid System Techniques
EDAT- 2009/10/23 06:00
MHDA- 2010/09/29 06:00
CRDT- 2009/10/23 06:00
PHST- 2009/04/14 00:00 [received]
PHST- 2009/09/09 00:00 [accepted]
PHST- 2009/10/23 06:00 [entrez]
PHST- 2009/10/23 06:00 [pubmed]
PHST- 2010/09/29 06:00 [medline]
AID - 10.1007/s10549-009-0581-0 [doi]
PST - ppublish
SO  - Breast Cancer Res Treat. 2010 Jul;122(2):395-407. doi: 10.1007/s10549-009-0581-0. 
      Epub 2009 Oct 22.