scholarly journals Truncated E-cadherin potentiates cell death in prostate epithelial cells

The Prostate ◽  
2005 ◽  
Vol 63 (3) ◽  
pp. 259-268 ◽  
Author(s):  
Jonathan Rios-Doria ◽  
Mark L. Day
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Prostate Epithelial Cells ◽  
E Cadherin

E-cadherin expression and PSA secretion in human prostate epithelial cells

2001 ◽  
Vol 29 (4) ◽  
pp. 287-292 ◽  
Author(s):  
Diane Krill ◽  
Angela Thomas ◽  
Su-Ping Wu ◽  
Rajiv Dhir ◽  
Michael J. Becich
Keyword(s):  
Epithelial Cells ◽  
Human Prostate ◽  
Prostate Epithelial Cells ◽  
E Cadherin

scholarly journals NF- B inhibition increases chemosensitivity to trichostatin A-induced cell death of Ki-Ras-transformed human prostate epithelial cells

2006 ◽  
Vol 27 (11) ◽  
pp. 2258-2268 ◽  
Author(s):  
O. Kwon ◽  
K. A Kim ◽  
S. O. Kim ◽  
R. Ha ◽  
W. K. Oh ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Trichostatin A ◽  
Human Prostate ◽  
Prostate Epithelial Cells

scholarly journals Constitutively Activated Stat3 Induces Tumorigenesis and Enhances Cell Motility of Prostate Epithelial Cells through Integrin β6

2007 ◽  
Vol 27 (12) ◽  
pp. 4444-4453 ◽  
Author(s):  
Janeen Azare ◽  
Kenneth Leslie ◽  
Hikmat Al-Ahmadie ◽  
William Gerald ◽  
Paul H. Weinreb ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Soft Agar ◽  
Cellular Migration ◽  
Mutant Form ◽  
Signal Transducer ◽  
Prostate Tumorigenesis ◽  
Prostate Epithelial Cells ◽  
Integrin Αvβ6 ◽  
Transcription 3 ◽  
E Cadherin

ABSTRACT The persistent activation of signal transducer and activator of transcription 3 (Stat3) is a common feature of prostate cancer. However, little is known about the Stat3 targets that may mediate prostate tumorigenesis. The introduction of an activating mutant form of Stat3 (Stat3-C) into immortalized prostate epithelial cells resulted in tumorigenesis. Stat3-C-expressing cells had decreased E-cadherin levels, increased numbers of lamellipodia and stress fibers, and enhanced migratory capacities compared to vector control-expressing cells, with a concomitant increase in the expression of integrin β6 and its ligand, fibronectin (FN). Exogenously added FN increased cellular migration, with a concomitant loss of E-cadherin expression. The blockade of integrin αvβ6 in Stat3-C-expressing cells inhibited migration, increased E-cadherin levels, and reduced colony formation in soft agar. These results demonstrate the sufficiency of constitutively activated Stat3 in mediating prostate tumorigenesis and identify novel Stat3 targets that are involved in promoting cell migration and transformation.

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