Abstract:
:Pro-inflammatory conditions have long been associated with mammary carcinogenesis and breast cancer progression. The underlying mechanisms are incompletely understood but signaling of pro-inflammatory cytokine TNFα through its receptors TNFR1 and TNFR2 is a major mediator of inflammation in both obesity and in the response of tissues to radiation, 2 known risk factors for the development of breast cancer. Here, we demonstrated the loss of one TNFR2 allele led to ductal hyperplasia in the mammary gland with increased numbers of mammary epithelial stem cell and terminal end buds. Furthermore, loss of one TNFR2 allele increased the incidence of breast cancer in MMTV-Wnt1 mice and resulted in tumors with a more aggressive phenotype and metastatic potential. The underlying mechanisms include a preferential activation of canonical NF-κB signaling pathway and autocrine production of TNFα. Analysis of the TCGA dataset indicated inferior overall survival for patients with down-regulated TNFR2 expression. These findings unravel the imbalances in TNFR signaling promote the development and progression of breast cancer, indicating that selective agonists of TNFR2 could potentially modulate the risk for breast cancer in high-risk populations.
journal_name
Neoplasiajournal_title
Neoplasia (New York, N.Y.)authors
He L,Bhat K,Duhacheck-Muggy S,Ioannidis A,Zhang L,Nguyen NT,Moatamed NA,Pajonk Fdoi
10.1016/j.neo.2020.12.007subject
Has Abstractpub_date
2021-02-01 00:00:00pages
197-209issue
2eissn
1522-8002issn
1476-5586pii
S1476-5586(20)30188-3journal_volume
23pub_type
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