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![New insights into acquired endocrine resistance of breast cancer](https://image.oaes.cc/fd87a57c-432d-471d-8264-f359fdebd573/3091.fig.3.jpg)
Figure 3. The protein kinase RNA-like endoplasmic reticulum kinase (PERK)/nuclear factor κB (NF-κB)/tumor necrosis factor α (TNFα) axis is activated by E2 to induce apoptosis in long term estrogen deprivation breast cancer cells. E2 activates nuclear estrogen receptor α (ERα) and accumulates unfolded proteins in the endoplasmic reticulum, which activates PERK in response to the misfolded proteins. This stress kinase phosphorylates signal transducer and activator of transcription 3 (STAT3) and increases its DNA-binding activity. Subsequently, activated STAT3 promotes NF-κB DNA binding and induction of TNFα expression[22]