New control of the senescence barrier in breast cancer

Abstract

Normal cells exposed to cancer-causing events respond by triggering cellular senescence, a stress response which halts cell proliferation and constitutes a protective anti-cancer barrier. We have uncovered a previously unknown signaling pathway implicating p21-activated kinase 4 (PAK4) in the control of senescence in breast cancer, via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) subunit RELB and the CCAAT-enhancer-binding protein beta (C/EBPβ).

Keywords

• cellular senescence
• p21-activated kinase
• pak4
• relb
• cebpb