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. 2018 Nov 29;16:92. doi: 10.1186/s12964-018-0304-4

Fig. 6.

Fig. 6

PTPRZ1 activated the NF-κB pathway in breast cancer cells following treatment with Dox. a RT-PCR analyses of the expression of NF-κB pathway components, including IKKα, IKKβ, IκBα, p65 and p50, in MDA-MB-231 cells transfected with PTPRZ1, siPTPRZ1 or scrambled siRNA (vector) and then treated with Dox (1 μg/ml) for 24 h are shown, n = 3, Student’s t-test, *p < 0.05, **p < 0.01, ***p < 0.001. b The phosphorylation of NF-κB pathway components was detected by western blotting; NF-κB activation was investigated by assessing the phosphorylation of IKKα/β (Ser176), IκBα (Ser32) and p65(Ser536). c Proposed model for mechanisms of CDKN1A/PTN/PTPRZ1-induced chemoresistance in breast cancer cells