scholarly journals Smac peptide potentiates TRAIL- or paclitaxel-mediated ovarian cancer cell death in vitro and in vivo

2012 ◽  
Vol 29 (2) ◽  
pp. 515-522 ◽  
Author(s):  
HONG LUAN MAO ◽  
YINGXIN PANG ◽  
XIAOLEI ZHANG ◽  
FANG YANG ◽  
JINGFANG ZHENG ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Death

A water-soluble analog of triptolide induces ovarian cancer cell death in vitro and in vivo

2013 ◽  
Vol 130 (1) ◽  
pp. e130
Author(s):  
C. Rivard Hunt ◽  
M. Geller ◽  
C. Evans ◽  
R. Vogel ◽  
S. Ramakrishnan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Water Soluble ◽  
Cancer Cell Death

Pre-clinical models of cellular therapy combined with cytokines demonstrate in vitro and in vivo ovarian cancer cell killing

2012 ◽  
Vol 125 ◽  
pp. S45
Author(s):  
S. Ingersoll ◽  
S. Ahmad ◽  
G. Stoltzfus ◽  
M. Merchant ◽  
A. Ahmed ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cell ◽  
Cellular Therapy ◽  
Ovarian Cancer Cell ◽  
Cell Killing ◽  
Clinical Models

Abstract 1865: Ciglitazone increases ovarian cancer cell death by inhibiting GLUT-1 expression.

2013 ◽  
Author(s):  
Jin Young Kim ◽  
So Jin Shin ◽  
Keon Uk Park ◽  
Young June Jeon ◽  
Chi Heum Cho ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Glut 1 ◽  
Cancer Cell Death

scholarly journals Involvement of general control nonderepressible kinase 2 in cancer cell apoptosis by posttranslational mechanisms

2015 ◽  
Vol 26 (6) ◽  
pp. 1044-1057 ◽  
Author(s):  
Chen Wei ◽  
Ma Lin ◽  
Bian Jinjun ◽  
Feng Su ◽  
Cao Dan ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Protein Level ◽  
Cell Apoptosis ◽  
General Control ◽  
Screening Assay ◽  
Cancer Cell Apoptosis ◽  
Cancer Cell Death

General control nonderepressible kinase 2 (GCN2) is a promising target for cancer therapy. However, the role of GCN2 in cancer cell survival or death is elusive; further, small molecules targeting GCN2 signaling are not available. By using a GCN2 level-based drug screening assay, we found that GCN2 protein level critically determined the sensitivity of the cancer cells toward Na+,K+-ATPase ligand–induced apoptosis both in vitro and in vivo, and this effect was largely dependent on C/EBP homologous protein (CHOP) induction. Further analysis revealed that GCN2 is a short-lived protein. In A549 lung carcinoma cells, cellular β-arrestin1/2 associated with GCN2 and maintained the GCN2 protein level at a low level by recruiting the E3 ligase NEDD4L and facilitating consequent proteasomal degradation. However, Na+,K+-ATPase ligand treatment triggered the phosphorylation of GCN2 at threonine 899, which increased the GCN2 protein level by disrupting the formation of GCN2–β-arrestin–NEDD4L ternary complex. The enhanced GCN2 level, in turn, aggravated Na+,K+-ATPase ligand–induced cancer cell apoptosis. Our findings reveal that GCN2 can exert its proapoptotic function in cancer cell death by posttranslational mechanisms. Moreover, Na+,K+-ATPase ligands emerge as the first identified small-molecule drugs that can trigger cancer cell death by modulating GCN2 signaling.

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