scholarly journals AKR1C3 Overexpression Mediates Methotrexate Resistance in Choriocarcinoma Cells

2014 ◽  
Vol 11 (11) ◽  
pp. 1089-1097 ◽  
Author(s):  
Jing Zhao ◽  
Yang Xiang ◽  
Changji Xiao ◽  
Peng Guo ◽  
Dan Wang ◽  
...  
1991 ◽  
Vol 266 (10) ◽  
pp. 6181-6187 ◽  
Author(s):  
D E McCloskey ◽  
J J McGuire ◽  
C A Russell ◽  
B G Rowan ◽  
J R Bertino ◽  
...  

1991 ◽  
Vol 266 (13) ◽  
pp. 8517-8522
Author(s):  
A. Hochberg ◽  
C. Sibley ◽  
M. Pixley ◽  
Y. Sadovsky ◽  
B. Strauss ◽  
...  

1985 ◽  
Vol 260 (27) ◽  
pp. 14732-14742 ◽  
Author(s):  
B P Peters ◽  
R J Hartle ◽  
R F Krzesicki ◽  
T G Kroll ◽  
F Perini ◽  
...  

1997 ◽  
Vol 11 (11) ◽  
pp. 1651-1658 ◽  
Author(s):  
Limin Liu ◽  
Douglas Leaman ◽  
Michel Villalta ◽  
R. Michael Roberts

Abstract CG is required for maintenance of the corpus luteum during pregnancy in higher primates. As CG is a heterodimeric molecule, some form of coordinated control must be maintained over the transcription of its two subunit genes. We recently found that expression of human CG β-subunit (hCGβ) in JAr human choriocarcinoma cells was almost completely silenced by the embryonic transcription factor Oct-3/4, which bound to a unique ACAATAATCA octameric sequence in the hCGβ gene promoter. Here we report that Oct-3/4 is also a potent inhibitor of hCG α-subunit (hCGα) expression in JAr cells. Oct-3/4 reduced human GH reporter expression from the −170 hCGα promoter in either the presence or absence of cAMP by about 70% in transient cotransfection assays, but had no effect on expression from either the −148 hCGα or the −99 hCGα promoter. Unexpectedly, no Oct-3/4-binding site was identified within the −170 to −148 region of the hCGα promoter, although one was found around position −115 by both methylation interference footprinting and electrophoretic mobility shift assays. Site-directed mutagenesis of this binding site destroyed the affinity of the promoter for Oct-3/4, but did not affect repression of the promoter. Therefore, inhibition of hCGα gene transcription by Oct-3/4 appears not to involve direct binding of this factor to the site responsible for silencing. When stably transfected into JAr cells, Oct-3/4 reduced the amounts of both endogenous hCGα mRNA and protein by 70–80%. Oct-3/4 is therefore capable of silencing both hCGα and hCGβ gene expression. We suggest that as the trophoblast begins to form, reduction of Oct-3/4 expression permits the coordinated onset of transcription from the hCGα and hCGβ genes.


1989 ◽  
Vol 264 (21) ◽  
pp. 12611-12619
Author(s):  
S Watanabe ◽  
T Watanabe ◽  
W B Li ◽  
B W Soong ◽  
J Y Chou

Endocrinology ◽  
1979 ◽  
Vol 104 (1) ◽  
pp. 8-16 ◽  
Author(s):  
E. R. SIMPSON ◽  
D. W. BILHEIMER ◽  
P. C. MACDONALD ◽  
J. C. PORTER

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