scholarly journals Tumor necrosis factor-α-induced a disintegrin and metalloprotease 10 increases apoptosis resistance in prostate cancer cells

2014 ◽  
Vol 7 (3) ◽  
pp. 897-901 ◽  
Author(s):  
LI BING ZHU ◽  
SHENG TAO ZHAO ◽  
TING ZHAO XU ◽  
HE WANG
Keyword(s):  
Prostate Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Prostate Cancer Cells ◽  
Apoptosis Resistance ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Analysis of tumor necrosis factor α-induced and nuclear factor κB-silenced LNCaP prostate cancer cells by RT-qPCR

2014 ◽  
Vol 8 (6) ◽  
pp. 1695-1700 ◽  
Author(s):  
CEREN GONEN-KORKMAZ ◽  
GULNUR SEVIN ◽  
GOKSEL GOKCE ◽  
MEHMET ZUHURI ARUN ◽  
GOKCE YILDIRIM ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Prostate Cancer Cells ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Fibronectin Protects Prostate Cancer Cells from Tumor Necrosis Factor-α-induced Apoptosis via the AKT/Survivin Pathway

2003 ◽  
Vol 278 (50) ◽  
pp. 50402-50411 ◽  
Author(s):  
Mara Fornaro ◽  
Janet Plescia ◽  
Sophie Chheang ◽  
Giovanni Tallini ◽  
Yong-M. Zhu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Prostate Cancer Cells ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Smac Mimetic Bypasses Apoptosis Resistance in FADD- or Caspase-8-Deficient Cells by Priming for Tumor Necrosis Factor α-Induced Necroptosis

Neoplasia ◽  
2011 ◽  
Vol 13 (10) ◽  
pp. 971-IN29 ◽  
Author(s):  
Bram Laukens ◽  
Claudia Jennewein ◽  
Barbara Schenk ◽  
Nele Vanlangenakker ◽  
Alexander Schier ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Caspase 8 ◽  
Apoptosis Resistance ◽  
Smac Mimetic ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Estradiol Abrogates Apoptosis in Breast Cancer Cells through Inactivation of BAD: Ras-dependent Nongenomic Pathways Requiring Signaling through ERK and Akt

2004 ◽  
Vol 15 (7) ◽  
pp. 3266-3284 ◽  
Author(s):  
Romaine Ingrid Fernando ◽  
Jay Wimalasena
Keyword(s):  
Breast Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Dominant Negative ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

Estrogens such as 17-β estradiol (E2) play a critical role in sporadic breast cancer progression and decrease apoptosis in breast cancer cells. Our studies using estrogen receptor-positive MCF7 cells show that E2 abrogates apoptosis possibly through phosphorylation/inactivation of the proapoptotic protein BAD, which was rapidly phosphorylated at S112 and S136. Inhibition of BAD protein expression with specific antisense oligonucleotides reduced the effectiveness of tumor necrosis factor-α, H2O2, and serum starvation in causing apoptosis. Furthermore, the ability of E2 to prevent tumor necrosis factor-α-induced apoptosis was blocked by overexpression of the BAD S112A/S136A mutant but not the wild-type BAD. BAD S112A/S136A, which lacks phosphorylation sites for p90RSK1 and Akt, was not phosphorylated in response to E2 in vitro. E2 treatment rapidly activated phosphatidylinositol 3-kinase (PI-3K)/Akt and p90RSK1 to an extent similar to insulin-like growth factor-1 treatment. In agreement with p90RSK1 activation, E2 also rapidly activated extracellular signal-regulated kinase, and this activity was down-regulated by chemical and biological inhibition of PI-3K suggestive of cross talk between signaling pathways responding to E2. Dominant negative Ras blocked E2-induced BAD phosphorylation and the Raf-activator RasV12T35S induced BAD phosphorylation as well as enhanced E2-induced phosphorylation at S112. Chemical inhibition of PI-3K and mitogen-activated protein kinase kinase 1 inhibited E2-induced BAD phosphorylation at S112 and S136 and expression of dominant negative Ras-induced apoptosis in proliferating cells. Together, these data demonstrate a new nongenomic mechanism by which E2 prevents apoptosis.

Mutant p53 Enhances Nuclear Factor κB Activation by Tumor Necrosis Factor α in Cancer Cells

2007 ◽  
Vol 67 (6) ◽  
pp. 2396-2401 ◽  
Author(s):  
Lilach Weisz ◽  
Alexander Damalas ◽  
Michalis Liontos ◽  
Panagiotis Karakaidos ◽  
Giulia Fontemaggi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Nuclear Factor Κb ◽  
Mutant P53 ◽  
Nuclear Factor ◽  
Factor Α ◽  
Necrosis Factor

Significance of Tumor Necrosis factor α-308 (G/A) gene polymorphism in the development of prostate cancer

2012 ◽  
Vol 39 (12) ◽  
pp. 11125-11130 ◽  
Author(s):  
Nega Berhane ◽  
Rabinder Chandera Sobti ◽  
Shiferaw Melesse ◽  
Salih Abdul Mahdi ◽  
Afework Kassu
Keyword(s):  
Prostate Cancer ◽  
Tumor Necrosis Factor ◽  
Gene Polymorphism ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor
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