Title : Deoxypodophyllotoxin triggers parthanatos in glioma cells via induction of excessive ROS.

Pub. Date : 2016 Feb 28

PMID : 26683770






4 Functional Relationships(s)
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1 We found that DPT induced glioma cell death in vitro and inhibited the growth of xenograft glioma in vivo, which was accompanied with parthanatos-related biochemical events including expressional upregulation of PARP-1, cytoplasmic accumulation of PAR polymer, and nuclear translocation of AIF. deoxypodophyllotoxin poly (ADP-ribose) polymerase family, member 1 Mus musculus
2 In vitro study revealed that genetic knockdown of PARP-1 with small interfering RNA attenuated DPT-induced elevation in the cytoplasmic PAR-polymer and the nuclear AIF, as well as protected glioma cells against the toxicity of DPT. deoxypodophyllotoxin poly (ADP-ribose) polymerase family, member 1 Mus musculus
3 In vitro study revealed that genetic knockdown of PARP-1 with small interfering RNA attenuated DPT-induced elevation in the cytoplasmic PAR-polymer and the nuclear AIF, as well as protected glioma cells against the toxicity of DPT. deoxypodophyllotoxin poly (ADP-ribose) polymerase family, member 1 Mus musculus
4 Further, antioxidant NAC, as well as PARP-1 inhibitor 3AB, not only alleviated the overproduction of ROS caused by DPT, but also reversed the above-mentioned biochemical events, maintained mitochondrial membrane potential and rescued glioma cells death. deoxypodophyllotoxin poly (ADP-ribose) polymerase family, member 1 Mus musculus