Abstract
New light on Smac mimetics and breast cancer.
Highlights
It has previously been described that cancer cell lines sensitive to Smac mimetics (SMs) as a single agent are dependent on autocrine TNFα production
The noncanonical NF-κB signaling pathway has been suggested as the mediator of SM-induced TNFα production.[3,4,5,10]
In MDA-MB-468 cells, SM induces the noncanonical pathway and gene expression (BIRC3 induction), but still no increase in TNFα. This raises the possibility that other pathways are critical for SM-mediated TNFα synthesis
Summary
It has previously been described that cancer cell lines sensitive to SM as a single agent are dependent on autocrine TNFα production. The noncanonical NF-κB signaling pathway has been suggested as the mediator of SM-induced TNFα production.[3,4,5,10] in MDA-MB-468 cells, SM induces the noncanonical pathway and gene expression (BIRC3 induction), but still no increase in TNFα.
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