New control of the senescence barrier in breast cancer.
Tânia D F CostaStaffan StrömbladPublished in: Molecular & cellular oncology (2020)
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).
Keyphrases
- nuclear factor
- binding protein
- toll like receptor
- signaling pathway
- induced apoptosis
- dna damage
- endothelial cells
- pi k akt
- cell proliferation
- cell cycle arrest
- stress induced
- transcription factor
- protein kinase
- oxidative stress
- childhood cancer
- squamous cell
- epithelial mesenchymal transition
- cell cycle
- endoplasmic reticulum stress
- inflammatory response
- immune response
- cell death
- lps induced
- young adults