PMID- 16273365
OWN - NLM
STAT- MEDLINE
DCOM- 20060223
LR  - 20051125
IS  - 0344-5704 (Print)
IS  - 0344-5704 (Linking)
VI  - 56 Suppl 1
DP  - 2005 Nov
TI  - Function of nuclear sex hormone receptors in gene regulation.
PG  - 4-9
AB  - The development of reproductive organ tumors such as breast and prostate cancer 
      often depends on the action of sex hormones. Nuclear sex hormone receptors are 
      members of the nuclear hormone receptor superfamily and act as ligand-inducible 
      transcription factors, controlling the expression of target genes. Nuclear 
      receptors are considered to directly and indirectly interact with a number of 
      nuclear co-regulatory complexes involved in chromatin remodeling and histone 
      modification. Moreover, many intracellular signalings via cell membrane receptors 
      are shown to modulate nuclear receptor-regulated transcription. We have shown 
      that estrogen receptors (ER) associate with a number of nuclear complexes, one of 
      which is a spliceosome complex. We recently found that this spliceosome complex 
      interacts with phosphorylated ER by MAP kinase, generating a novel cross-talk of 
      estrogen and growth factor signalings. We also observed that a dioxin receptor 
      (AhR) is capable of associating with ER, resulting in modulation of ER 
      transactivation function. From our findings we believe that development of 
      estrogen-dependent breast cancer may be mediated through the other signaling 
      pathways. To address the function of the androgen receptor (AR) in 
      androgen-dependent prostate cancer, we established a transgenic mouse line 
      expressing a human AR mutant that is found in androgen-independent prostate 
      cancer patients. The hAR mutant mice, generated through a Cre-loxP system, 
      developed hyperplasia in the prostates. Hypersensitivity of AR mutants to 
      antagonists and endogenous steroid hormones may potentiate hormone-dependency in 
      prostate cancer development.
FAU - Kato, Shigeaki
AU  - Kato S
AD  - Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 
      Yayoi, Bunkyo-ku, Tokyo, 113-0032, Japan. uskato@mail.ecc.u-tokyo.ac.jp
FAU - Sato, Takashi
AU  - Sato T
FAU - Watanabe, Tomoyuki
AU  - Watanabe T
FAU - Takemasa, Sayuri
AU  - Takemasa S
FAU - Masuhiro, Yoshikazu
AU  - Masuhiro Y
FAU - Ohtake, Fumiaki
AU  - Ohtake F
FAU - Matsumoto, Takahiro
AU  - Matsumoto T
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Cancer Chemother Pharmacol
JT  - Cancer chemotherapy and pharmacology
JID - 7806519
RN  - 0 (Estrogens)
RN  - 0 (Growth Substances)
RN  - 0 (Receptors, Androgen)
RN  - 0 (Receptors, Estrogen)
SB  - IM
MH  - Animals
MH  - Estrogens/pharmacology
MH  - Gene Expression Regulation/drug effects/*physiology
MH  - Growth Substances/pharmacology
MH  - Humans
MH  - Models, Biological
MH  - Receptors, Androgen/*physiology
MH  - Receptors, Estrogen/*physiology
RF  - 28
EDAT- 2005/11/08 09:00
MHDA- 2006/02/24 09:00
CRDT- 2005/11/08 09:00
PHST- 2005/11/08 09:00 [pubmed]
PHST- 2006/02/24 09:00 [medline]
PHST- 2005/11/08 09:00 [entrez]
AID - 10.1007/s00280-005-0102-8 [doi]
PST - ppublish
SO  - Cancer Chemother Pharmacol. 2005 Nov;56 Suppl 1:4-9. doi: 
      10.1007/s00280-005-0102-8.