Identification and characterization of the binding properties of steroid hormone receptors in the nuclear fraction of adenomas of the human prostate gland

1982 ◽  
Vol 12 (6) ◽  
pp. 484-488
Author(s):  
Ts. I. Gerasimova ◽  
A. N. Smirnov ◽  
A. F. Bunyatyan

1986 ◽  
Vol 10 (5) ◽  
pp. 737-743 ◽  
Author(s):  
Prabir K. Chaudhuri ◽  
Nili Patel ◽  
Leslye Sandberg ◽  
Richard A. Prinz


2014 ◽  
Vol 191 (4S) ◽  
Author(s):  
João C.C. Alonso ◽  
Patrick V. Garcia ◽  
Leonardo O. Reis ◽  
Ubirajara Ferreira ◽  
Wagner E. Matheus ◽  
...  


1987 ◽  
Vol 113 (3) ◽  
pp. 285-290 ◽  
Author(s):  
A. Reiner ◽  
R. Kolb ◽  
G. Reiner ◽  
R. Jakesz ◽  
M. Schemper ◽  
...  


1985 ◽  
Vol 22 (1) ◽  
pp. 85-90 ◽  
Author(s):  
A.O. Brinkmann ◽  
J.Bolt-de Vries ◽  
W. de Boer ◽  
L.M. Lindh ◽  
E. Mulder ◽  
...  


Author(s):  
Eduardo M. Belotti ◽  
Sofía C. Sacco ◽  
Antonela F. Stassi ◽  
Ulises S. Notaro ◽  
Emmanuel Angeli ◽  
...  


2006 ◽  
Vol 34 (6) ◽  
pp. 1089-1094 ◽  
Author(s):  
G. Verrijdt ◽  
T. Tanner ◽  
U. Moehren ◽  
L. Callewaert ◽  
A. Haelens ◽  
...  

The AR (androgen receptor) is a hormone-dependent transcription factor that translates circulating androgen hormone levels into a physiological cellular response by directly regulating the expression of its target genes. It is the key molecule in e.g. the development and maintenance of the male sexual characteristics, spermatocyte production and prostate gland development and growth. It is also a major factor in the onset and maintenance of prostate cancer and a first target for pharmaceutical action against the further proliferation of prostate cancer cells. The AR is a member of the steroid hormone receptors, a group of steroid-inducible transcription factors sharing an identical consensus DNA-binding motif. The problem of how specificity in gene activation is achieved among the different members of this nuclear receptor subfamily is still unclear. In this report, we describe our investigations on how the AR can specifically activate its target genes, while the other steroid hormone receptors do not, despite having the same consensus monomeric DNA-binding motif. In this respect, we describe how the AR interacts with a newly identified class of steroid-response elements to which only the AR and not, for example, the glucocorticoid receptor can bind.



2011 ◽  
Author(s):  
Yamilet Noriega ◽  
Miguel Rivas ◽  
Elizabeth Langley


2018 ◽  
Vol 40 (3) ◽  
pp. 184-189 ◽  
Author(s):  
T V Zadvornyi ◽  
N Yu Lukianova ◽  
T V Borikun ◽  
V F Chekhun

Aim: To investigate the biological effects of exogenous lactoferrin (LF) on phenotypic profile and invasiveness of human prostate cancer (PC) cells in vitro. Materials and Methods: Human PC cell lines (LNCaP, DU-145) were cultured with an exogenous LF at a dose corresponding to IC30. The expression levels of steroid hormone receptors (androgen receptor, estrogen receptor, progesterone receptor), Her2/neu, Ki-67, E- and N-cadherin, were monitored by immunohistochemical analysis. The levels of miRNAs were assessed using q-PCR. The invasive activity of the cells was examined in a standard invasion test. Results: Exogenous LF reduced expression of steroid hormone receptors (ERα and PR) and Ki-67 in both PC cell lines. The expression of E-cadherin increased significantly in LF-treated DU-145 cells. Also, we established the decrease in invasive activity upon LF treatment by 40% and 30% in DU-145 and LNCaP cells, respectively. In DU-145 cells, incubation with exogenous LF resulted in an increase in the expression of oncosuppressive (miR-133a and miR-200b) miRNAs. Conclusions: Exogenous LF causes the changes in phenotypic characteristics of PC cells and levels of oncogenic and oncosuppressive miRNAs involved in the regulation of key cellular processes.



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