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. 2020 Apr 22;10:584. doi: 10.3389/fonc.2020.00584

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Copyright © 2020 Mercogliano, Bruni, Elizalde and Schillaci.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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TNFα signaling in luminal breast cancer cells. TNFα binds to TNFR1 and induces the activation of PI3K/Akt, p42/p44MAPK and JNK, while its binding to TNFR2 mainly induces p42/p44MAPK activation. PI3K/Akt and JNK then activates NF-κB that promotes the transcription of cyclin D1 and the consequent cell proliferation. In addition, NF-κB also induces the expression of TNFα, establishing a positive feed-back. E2 binds to ER and also promotes luminal cancer cell proliferation through cyclin D1 upregulation by tethering NF-κB and enhances its activity. sTNFα, soluble TNFα; TNFR1, TNFα receptor 1; TNFR2, TNFα receptor 2; E2, estradiol; ER, estrogen receptor.