PMID- 10625666
OWN - NLM
STAT- MEDLINE
DCOM- 20000218
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 275
IP  - 2
DP  - 2000 Jan 14
TI  - PDEF, a novel prostate epithelium-specific ets transcription factor, interacts
      with the androgen receptor and activates prostate-specific antigen gene
      expression.
PG  - 1216-25
AB  - Prostate cancer, the most frequent solid cancer in older men, is a leading cause 
      of cancer deaths. Although proliferation and differentiation of normal prostate
      epithelia and the initial growth of prostate cancer cells are androgen-dependent,
      prostate cancers ultimately become androgen-independent and refractory to hormone
      therapy. The prostate-specific antigen (PSA) gene has been widely used as a
      diagnostic indicator for androgen-dependent and -independent prostate cancer.
      Androgen-induced and prostate epithelium-specific PSA expression is regulated by 
      a proximal promoter and an upstream enhancer via several androgen receptor
      binding sites. However, little progress has been made in identifying
      androgen-independent regulatory elements involved in PSA gene regulation. We
      report the isolation of a novel, prostate epithelium-specific Ets transcription
      factor, PDEF (prostate-derived Ets factor), that among the Ets family uniquely
      prefers binding to a GGAT rather than a GGAA core. PDEF acts as an
      androgen-independent transcriptional activator of the PSA promoter. PDEF also
      directly interacts with the DNA binding domain of androgen receptor and enhances 
      androgen-mediated activation of the PSA promoter. Our results, as well as the
      critical roles of other Ets factors in cellular differentiation and
      tumorigenesis, strongly suggest that PDEF is an important regulator of prostate
      gland and/or prostate cancer development.
FAU - Oettgen, P
AU  - Oettgen P
AD  - New England Baptist Bone and Joint Institute, Beth Israel Deaconess Medical
      Center and Harvard Medical School, Boston, Massachusetts 02115, USA.
FAU - Finger, E
AU  - Finger E
FAU - Sun, Z
AU  - Sun Z
FAU - Akbarali, Y
AU  - Akbarali Y
FAU - Thamrongsak, U
AU  - Thamrongsak U
FAU - Boltax, J
AU  - Boltax J
FAU - Grall, F
AU  - Grall F
FAU - Dube, A
AU  - Dube A
FAU - Weiss, A
AU  - Weiss A
FAU - Brown, L
AU  - Brown L
FAU - Quinn, G
AU  - Quinn G
FAU - Kas, K
AU  - Kas K
FAU - Endress, G
AU  - Endress G
FAU - Kunsch, C
AU  - Kunsch C
FAU - Libermann, T A
AU  - Libermann TA
LA  - eng
SI  - GENBANK/AF071538
GR  - R29 CA070297/CA/NCI NIH HHS/United States
GR  - KO8/CA 71429/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-ets)
RN  - 0 (Recombinant Proteins)
RN  - 0 (SPDEF protein, human)
RN  - 0 (Transcription Factors)
RN  - EC 3.4.21.77 (Prostate-Specific Antigen)
SB  - IM
MH  - Amino Acid Sequence
MH  - Base Sequence
MH  - Binding Sites
MH  - Cell Line
MH  - Cells, Cultured
MH  - *Gene Expression Regulation
MH  - Humans
MH  - Keratinocytes
MH  - Male
MH  - Molecular Sequence Data
MH  - Promoter Regions, Genetic
MH  - Prostate/*metabolism
MH  - Prostate-Specific Antigen/*genetics
MH  - Proto-Oncogene Proteins/chemistry/*genetics/metabolism
MH  - Proto-Oncogene Proteins c-ets
MH  - Recombinant Proteins/metabolism
MH  - Sequence Alignment
MH  - Sequence Homology, Amino Acid
MH  - Transcription Factors/chemistry/*genetics/*metabolism
MH  - Transcriptional Activation
MH  - Tumor Cells, Cultured
EDAT- 2000/01/08 09:00
MHDA- 2000/02/26 09:00
CRDT- 2000/01/08 09:00
PHST- 2000/01/08 09:00 [pubmed]
PHST- 2000/02/26 09:00 [medline]
PHST- 2000/01/08 09:00 [entrez]
AID - 10.1074/jbc.275.2.1216 [doi]
AID - S0021-9258(18)31238-9 [pii]
PST - ppublish
SO  - J Biol Chem. 2000 Jan 14;275(2):1216-25. doi: 10.1074/jbc.275.2.1216.