Open AccessTAp73 represses NF-κB–mediated recruitment of tumor-associated macrophages in breast cancer
Author(s) -
Johanna Wolfsberger,
Habib A. M. Sakil,
Leilei Zhou,
Niek van Bree,
Elena Baldisseri,
Sabrina de Souza Ferreira,
Verónica Zubillaga,
Marina Stantic,
Nicolas Fritz,
Johan Hartman,
Charlotte Rolny,
Margareta Wilhelm
Publication year - 2021
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2017089118
Subject(s) - ccl2 , breast cancer , chemokine , cancer research , infiltration (hvac) , immune system , biology , macrophage , regulator , cancer , nf κb , disease , immunology , inflammation , medicine , gene , biochemistry , in vitro , thermodynamics , physics
Significance Breast cancer is one of the most prevalent cancers worldwide. Understanding this complex disease is therefore of great importance. Here, we report that loss of TAp73, a known tumor suppressor and member of the p53 protein family, leads to increased activation of the NF-κB pathway, secretion of the chemokine CCL2, and an increase in protumoral macrophage infiltration in human breast cancer. Both high levels of CCL2 and high macrophage infiltration are known to correlate with poor prognosis in breast cancer patients. This study identifies TAp73 as a regulator of macrophage recruitment and highlights a role for TAp73 in immune cell regulation in cancer.
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