Title : The role of p38 MAPK and JNK in Arsenic trioxide-induced mitochondrial cell death in human cervical cancer cells.

Pub. Date : 2008 Oct

PMID : 18412143






6 Functional Relationships(s)
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1 As2O3-induced apoptotic cell death in HeLa cells was associated with activation and mitochondrial translocation of Bax, a marked phosphorylation of Bcl-2, reduction of Bcl-2 and Bax interaction, dissipation of mitochondrial membrane potential. Arsenic Trioxide BCL2 associated X, apoptosis regulator Homo sapiens
2 As2O3-induced apoptotic cell death in HeLa cells was associated with activation and mitochondrial translocation of Bax, a marked phosphorylation of Bcl-2, reduction of Bcl-2 and Bax interaction, dissipation of mitochondrial membrane potential. Arsenic Trioxide BCL2 associated X, apoptosis regulator Homo sapiens
3 Using small interfering RNA, reduced Bax expression effectively attenuated As2O3-induced mitochondrial membrane potential loss and apoptotic cell death. Arsenic Trioxide BCL2 associated X, apoptosis regulator Homo sapiens
4 Moreover, the phosphorylation of Bcl-2 induced by As2O3 diminished its ability to bind to Bax. Arsenic Trioxide BCL2 associated X, apoptosis regulator Homo sapiens
5 In addition, N-acetyl-L-cystein (NAC), a thiol-containing anti-oxidant, completely blocked As2O3-induced p38 MAPK and JNK activations, mitochondria translocation of Bax, and phosphorylation of Bcl-2. Arsenic Trioxide BCL2 associated X, apoptosis regulator Homo sapiens
6 These results support a notion that ROS-mediated activations of p38 MAPK and JNK in response to As2O3 treatment signals activation of Bax and phosphorylation of Bcl-2, resulting in mitochondrial apoptotic cell death in human cervical cancer cells. Arsenic Trioxide BCL2 associated X, apoptosis regulator Homo sapiens