PMID- 17342330
OWN - NLM
STAT- MEDLINE
DCOM- 20070607
LR  - 20201214
IS  - 1021-335X (Print)
IS  - 1021-335X (Linking)
VI  - 17
IP  - 4
DP  - 2007 Apr
TI  - Differential regulation of DEC2 among hypoxia-inducible genes in endometrial 
      carcinomas.
PG  - 871-8
AB  - In this study, we demonstrate an important role of activation of the 
      hypoxia-inducible factor-1 (HIF-1) pathway in endometrial carcinogenesis and 
      tumor phenotype development of endometrial carcinoma, and suggest a unique role 
      of the HIF-1-target gene, differentiated embryo chondrocyte 2 (DEC2), in 
      carcinogenesis. Hypoxia caused an increase in HIF-1alpha protein expression in 4 
      endometrial carcinoma cell lines. The expressions of its 5 target genes - DEC1, 
      DEC2, carbonic anhydrase-9 (CA9), vascular endothelial growth factor (VEGF), and 
      solute carrier family 2, member 1 (SLC2A1) - also reactively increased in most of 
      the cell lines, except for DEC2 in the SNG-M cells. The expression levels of 
      DEC2, CA9, and SLC2A1 were significantly higher in the 4 atypical hyperplasia 
      tissues and 82 endometrial carcinomas compared with those in the 21 normal 
      endometria. Clinicopathological analyses of carcinoma patients revealed a 
      significant correlation of the VEGF and SLC2A1 expression with the status of 
      lymph-vascular involvement and lymph node metastasis. The expression levels of 
      CA9 and VEGF were significantly higher in the tumors of post- as opposed to 
      pre-menopausal patients. The SLC2A1 expression was also related to the FIGO 
      stage, but the DEC2 expression was inversely related to the FIGO grade. The 
      activation of the HIF-1 pathway could be related to endometrial carcinogenesis, 
      and the component, DEC2, could have different expression-regulatory mechanisms 
      and unique roles in carcinogenesis.
FAU - Yunokawa, Mayu
AU  - Yunokawa M
AD  - Department of Translational Cancer Research, Research Institute for Radiation 
      Biology and Medicine, Hiroshima University, Hiroshima 734-8553, Japan.
FAU - Tanimoto, Keiji
AU  - Tanimoto K
FAU - Nakamura, Hideaki
AU  - Nakamura H
FAU - Nagai, Nobutaka
AU  - Nagai N
FAU - Kudo, Yoshiki
AU  - Kudo Y
FAU - Kawamoto, Takeshi
AU  - Kawamoto T
FAU - Kato, Yukio
AU  - Kato Y
FAU - Hiyama, Eiso
AU  - Hiyama E
FAU - Hiyama, Keiko
AU  - Hiyama K
FAU - Nishiyama, Masahiko
AU  - Nishiyama M
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (BHLHE41 protein, human)
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (DELEC1 protein, human)
RN  - 0 (Glucose Transporter Type 1)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (SLC2A1 protein, human)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - EC 4.2.1.1 (CA9 protein, human)
RN  - EC 4.2.1.1 (Carbonic Anhydrase IX)
RN  - EC 4.2.1.1 (Carbonic Anhydrases)
SB  - IM
MH  - Antigens, Neoplasm/genetics
MH  - Basic Helix-Loop-Helix Transcription Factors/*genetics
MH  - Carbonic Anhydrase IX
MH  - Carbonic Anhydrases/genetics
MH  - Carcinoma/*genetics/metabolism/pathology
MH  - Endometrial Neoplasms/*genetics/metabolism/pathology
MH  - Female
MH  - Gene Expression Profiling
MH  - *Gene Expression Regulation, Neoplastic
MH  - Genes, Neoplasm/*genetics
MH  - Glucose Transporter Type 1/genetics
MH  - Humans
MH  - Hypoxia/*genetics/metabolism
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism
MH  - Tumor Cells, Cultured
MH  - Tumor Suppressor Proteins/genetics
MH  - Vascular Endothelial Growth Factor A/genetics
EDAT- 2007/03/08 09:00
MHDA- 2007/06/08 09:00
CRDT- 2007/03/08 09:00
PHST- 2007/03/08 09:00 [pubmed]
PHST- 2007/06/08 09:00 [medline]
PHST- 2007/03/08 09:00 [entrez]
PST - ppublish
SO  - Oncol Rep. 2007 Apr;17(4):871-8.