Chemotherapy-driven increases in the CDKN1A/PTN/PTPRZ1 axis promote chemoresistance by activating the NF-κB pathway in breast cancer cells.

We found that the levels of phosphorylated NF-κB pathway components, such as p-IKKα/β (Ser176), p-IκBα (Ser32) and p-p65(Ser536), were increased after NF-κB activation, while non-phosphorylated NF-κB components were unaffected or showed a trend towards reduced levels (Fig. 6 b).

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