scholarly journals Mono-galloyl glucose derivatives are potent poly(ADP-ribose) glycohydrolase (PARG) inhibitors and partially reduce PARP-1-dependent cell death

2008 ◽  
Vol 155 (8) ◽  
pp. 1235-1249 ◽  
Author(s):  
L Formentini ◽  
P Arapistas ◽  
M Pittelli ◽  
M Jacomelli ◽  
V Pitozzi ◽  
...  
Keyword(s):  
Cell Death ◽  
Dependent Cell ◽  
Parp 1 ◽  
Glucose Derivatives ◽  
Galloyl Glucose

scholarly journals AEBP1 down regulation induced cell death pathway depends on PTEN status of glioma cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Swati Sinha ◽  
Arun Renganathan ◽  
Prathima B. Nagendra ◽  
Vasudeva Bhat ◽  
Brian Steve Mathew ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cellular Proliferation ◽  
Ectopic Expression ◽  
Glioma Cells ◽  
Down Regulation ◽  
Over Expression ◽  
Cell Death Pathway ◽  
Dependent Cell ◽  
Parp 1

Abstract Glioblastoma (GBM) is the most common aggressive form of brain cancer with overall dismal prognosis (10–12 months) despite all current multimodal treatments. Previously we identified adipocyte enhancer binding protein 1 (AEBP1) as a differentially regulated gene in GBM. On probing the role of AEBP1 over expression in glioblastoma, we found that both cellular proliferation and survival were affected upon AEBP1 silencing in glioma cells, resulting in cell death. In the present study we report that the classical caspase pathway components are not activated in cell death induced by AEBP1 down regulation in PTEN-deficient (U87MG and U138MG) cells. PARP-1 was not cleaved but over-activated under AEBP1 down regulation which leads to the synthesis of PAR in the nucleus triggering the release of AIF from the mitochondria. Subsequently, AIF translocates to the nucleus along with MIF causing chromatinolysis. AEBP1 positively regulates PI3KinaseCβ by the binding to AE-1 binding element in the PI3KinaseCβ promoter. Loss of PI3KinaseCβ expression under AEBP1 depleted condition leads to excessive DNA damage and activation of PARP-1. Furthermore, over expression of PIK3CB (in trans) in U138MG cells prevents DNA damage in these AEBP1 depleted cells. On the contrary, AEBP1 down regulation induces caspase-dependent cell death in PTEN-proficient (LN18 and LN229) cells. Ectopic expression of wild-type PTEN in PTEN-deficient U138MG cells results in the activation of canonical caspase and Akt dependent cell death. Collectively, our findings define AEBP1 as a potential oncogenic driver in glioma, with potential implications for therapeutic intervention.

scholarly journals Calpain activation is not required for AIF translocation in PARP-1-dependent cell death (parthanatos)

2009 ◽  
Vol 110 (2) ◽  
pp. 687-696 ◽  
Author(s):  
Yingfei Wang ◽  
No S. Kim ◽  
Xiaoling Li ◽  
Peter A. Greer ◽  
Raymond C. Koehler ◽  
...  
Keyword(s):  
Cell Death ◽  
Calpain Activation ◽  
Dependent Cell ◽  
Parp 1

scholarly journals Discovery of pyrano[2,3-d]pyrimidine-2,4-dione derivatives as novel PARP-1 inhibitors: design, synthesis and antitumor activity

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4454-4464
Author(s):  
Nour E. A. Abd El-sattar ◽  
Eman H. K. Badawy ◽  
Eman Z. Elrazaz ◽  
Nasser S. M. Ismail
Keyword(s):  
Cell Death ◽  
Dna Repair ◽  
Antitumor Activity ◽  
Cancer Cell ◽  
Cytotoxic Agents ◽  
Repair Mechanism ◽  
Design Synthesis ◽  
Parp 1

PARP-1 are involved in DNA repair damage and so PARP-1 inhibitors have been used as potentiators in combination with DNA damaging cytotoxic agents to compromise the cancer cell DNA repair mechanism, resulting in genomic dysfunction and cell death.

Sign in / Sign up

Export Citation Format

Share Document