fig4

Figure 4. Regulation of nuclear factor κB (NF-κB) DNA-binding activity by other transcription factors in acquired resistant breast cancer cells. E₂/estrogen receptor α (ERα) activates endoplasmic reticulum stress and subsequently increases NF-κB DNA-binding activity. However, lipid metabolism-associated transcription factors CCAAT/enhancer binding protein β (C/EBP β) and peroxisome proliferator-activated receptor γ (PPARγ) and inflammation modulator GR all suppress the DNA-binding activity of NF-κB, thereby inhibition of E₂-induced apoptosis in long term estrogen deprivation breast cancer cells