Title : A combination of sulindac and arsenic trioxide synergistically induces apoptosis in human lung cancer H1299 cells via c-Jun NH2-terminal kinase-dependent Bcl-xL phosphorylation.

Pub. Date : 2008 Sep

PMID : 18281123






5 Functional Relationships(s)
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Protein Name
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1 A combination of sulindac and arsenic trioxide synergistically induces apoptosis in human lung cancer H1299 cells via c-Jun NH2-terminal kinase-dependent Bcl-xL phosphorylation. Arsenic Trioxide BCL2 like 1 Homo sapiens
2 Interestingly, a slower migrating Bcl-xL band was observed on immunoblots after treatment of cells with sulindac/ATO. Arsenic Trioxide BCL2 like 1 Homo sapiens
3 Treatment with SP600125 and transfection with DN-JNK blocked Bcl-xL phosphorylation, suggesting that JNK plays an important role in sulindac/ATO-induced Bcl-xL phosphorylation. Arsenic Trioxide BCL2 like 1 Homo sapiens
4 Treatment with SP600125 and transfection with DN-JNK blocked Bcl-xL phosphorylation, suggesting that JNK plays an important role in sulindac/ATO-induced Bcl-xL phosphorylation. Arsenic Trioxide BCL2 like 1 Homo sapiens
5 In conclusion, in H1299 human NSCLC cells, sulindac and ATO synergistically induce a high degree of apoptosis, which is mediated by the ROS-dependent JNK activation pathway via Bcl-xL phosphorylation. Arsenic Trioxide BCL2 like 1 Homo sapiens