Title : Extrinsic pathway- and cathepsin-dependent induction of mitochondrial dysfunction are essential for synergistic flavopiridol and vorinostat lethality in breast cancer cells.

Pub. Date : 2007 Dec

PMID : 18065490






4 Functional Relationships(s)
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Compound Name
Protein Name
Organism
1 Flavopiridol suppressed c-FLIP-l/s and BCL-xL expression, whereas vorinostat reduced expression of BCL-xL, and combined exposure to flavopiridol and vorinostat reduced MCL-1 and X-chromosome-linked inhibitor of apoptosis protein (XIAP) levels. alvocidib BCL2 like 1 Homo sapiens
2 Flavopiridol suppressed c-FLIP-l/s and BCL-xL expression, whereas vorinostat reduced expression of BCL-xL, and combined exposure to flavopiridol and vorinostat reduced MCL-1 and X-chromosome-linked inhibitor of apoptosis protein (XIAP) levels. alvocidib BCL2 like 1 Homo sapiens
3 Flavopiridol suppressed extracellular signal-regulated kinase 1/2 (ERK1/2) and AKT activity and expression of activated forms of AKT and mitogen-activated protein/ERK kinase 1 maintained c-FLIP-l/s, BCL-xL, and XIAP expression and protected cells against flavopiridol/vorinostat lethality. alvocidib BCL2 like 1 Homo sapiens
4 Overexpression of c-FLIP-s and BCL-xL abolished the lethality of flavopiridol/vorinostat. alvocidib BCL2 like 1 Homo sapiens