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Fig. 2 | BMC Cancer

Fig. 2

From: IΚΚε cooperates with either MEK or non-canonical NF-kB driving growth of triple-negative breast cancer cells in different contexts

Fig. 2

IKKε supports viability and MEK activation. a) 30 μg of protein was analyzed in whole cell lysates of breast cancer cells grown to 70% confluence. Cells were treated with vehicle control (Ctl), 2 μM MEK inhibitor (MEKi), 2 μM IKKβ inhibitor (IKKβi), or 2 μM BX795 for inhibition of IKKε (IKKεi) for 6 h before lysate collection. b) 30 μg of protein was analyzed in whole cell lysates of breast cancer cells grown to 70% confluence after siRNA mediated knockdown of IKBKE (siIKKε). Quantification of three independent replicates reveals increased non-canonical NF-κB proteins with IKBKE knockdown. c) 30 μg of protein was analyzed in whole cell lysates of MDA MB 468 cells after 1 h exposure to 2 μM BX795 for IKKε inhibition. Quantification of three independent replicates confirms pharmacological inhibition of IKKε activity significantly increased non-canonical NF-κB protein levels. *significantly different from corresponding vehicle control P < 0.05, unpaired T-test (b-c)

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