In vivo imaging of nuclear-cytoplasmic deformation and partition during cancer cell death due to immune rejection

2012 ◽  
Vol 113 (2) ◽  
pp. 465-472 ◽  
Author(s):  
Yasuyuki Amoh ◽  
Yuko Hamada ◽  
Kensei Katsuoka ◽  
Robert M. Hoffman
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
In Vivo Imaging ◽  
Immune Rejection ◽  
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.

pH-Triggered burst intracellular release from hollow microspheres to induce autophagic cancer cell death

2015 ◽  
Vol 3 (48) ◽  
pp. 9383-9396 ◽  
Author(s):  
Xin Liang ◽  
Ying Yang ◽  
Lijun Wang ◽  
Xianbing Zhu ◽  
Xiaowei Zeng ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Hollow Microspheres ◽  
Cancer Cell Death ◽  
Intracellular Release

Rapamycin–NaHCO3-loaded HMs combined CQ–NaHCO3-loaded HMs could efficiently induce cancer cell death through apoptosis with autophagosome both in vitro and in vivo.

scholarly journals Proanthocyanidin Polymer-Rich Fraction of Stryphnodendron adstringens Promotes in Vitro and in Vivo Cancer Cell Death via Oxidative Stress

2018 ◽  
Vol 9 ◽  
Author(s):  
Vanessa Kaplum ◽  
Anelise C. Ramos ◽  
Marcia E. L. Consolaro ◽  
Maria A. Fernandez ◽  
Tânia Ueda-Nakamura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cancer Cell ◽  
Cancer Cell Death

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
Sign in / Sign up

Export Citation Format

Share Document