Fig. 7: ETV7 can compete with STAT3 in the regulation of the TNFRSF1A gene influencing the NF-κB regulatory pathway.
From: ETV7 reduces inflammatory responses in breast cancer cells by repressing the TNFR1/NF-κB axis
A The canonical STAT3/TNF-α/NF-κB regulatory pathway. STAT3 binds to its regulatory element in the first intron of the TNFRSF1A gene and induces its expression by recruiting chromatin remodelers that result in an “active” state. Consequently, the TNF-α receptor 1 is produced. TNF-α molecules bind the TNFR1 receptor and activate the NF-κB signaling pathway. B In the context where ETV7 expression is increased, ETV7 can displace STAT3 from its binding sites on the Intron 1 of TNFRSF1A and directly represses its expression by altering the deposition of histone marks. This ETV7-mediated repression leads to the reduced activation of NF-κB signaling and, hence, reduces the expression of pro-inflammatory genes.
