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![New insights into acquired endocrine resistance of breast cancer](https://image.oaes.cc/fd87a57c-432d-471d-8264-f359fdebd573/3091.fig.4.jpg)
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