Fig. 7: PERK is a key driver to activate STAT3/NF-κB/TNFα axis in E2-deprived breast cancer cells. | Cell Death Discovery

Fig. 7: PERK is a key driver to activate STAT3/NF-κB/TNFα axis in E2-deprived breast cancer cells.

From: Modulation of nuclear factor-kappa B activation by the endoplasmic reticulum stress sensor PERK to mediate estrogen-induced apoptosis in breast cancer cells

Fig. 7

Nuclear E2/ER preferentially activates C/EBPβ which can suppress NF-κB DNA binding. E2 also activates PERK in response to the accumulation of unfolded proteins in the endoplasmic reticulum. This stress kinase activates transcription factor STAT3 to increase NF-κB DNA binding which results in induction of TNF family members and associated apoptosis. Additionally, PERK regulates Nrf2 and serves as a contact site between endoplasmic reticulum and mitochondria or interacts with mitochondria via Bim/Ca2+ to activate oxidative stress-related apoptosis

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