Triple-negative breast cancer influences a mixed M1/M2 macrophage phenotype associated with tumor aggressiveness.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2022
Historique:
received: 17 12 2021
accepted: 02 08 2022
entrez: 12 8 2022
pubmed: 13 8 2022
medline: 17 8 2022
Statut: epublish

Résumé

Triple-negative breast cancer (TNBC) is characterized by excessive accumulation of tumor-infiltrating immune cells, including tumor-associated macrophages (TAMs). TAMs consist of a heterogeneous population with high plasticity and are associated with tumor aggressiveness and poor prognosis. Moreover, breast cancer cells can secrete factors that influence TAM polarization. Therefore, this study aimed to evaluate the crosstalk between cancer cells and macrophages in the context of TNBC. Cytokine-polarized M2 macrophage were used as control. Distinct from the classical M2 macrophage, TAMs generated from TNBC-conditioned media upregulated both M1- and M2-associated genes, and secreted both the anti-inflammatory cytokine interleukin IL-10 and the proinflammatory cytokine IL-6 and tumor necrosis factor- α. Theses TNBC-induced TAMs exert aggressive behavior of TNBC cells. Consistently, TCGA and MTABRIC analyses of human breast cancer revealed upregulation of M1- associated genes in TNBC comparing with non-TNBC. Among these M1-associated genes, CXCL10 and IL1B were revealed to be independent prognostic factors for disease progression. In conclusion, TNBC cells induce macrophage polarization with a mixture of M1 and M2 phenotypes. These cancer-induced TAMs further enhance tumor cell growth and aggressiveness.

Identifiants

pubmed: 35960749
doi: 10.1371/journal.pone.0273044
pii: PONE-D-21-39755
pmc: PMC9374254
doi:

Substances chimiques

Cytokines 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0273044

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Kristine Cate S Pe (KCS)

Faculty of Pharmaceutical Sciences, Department of Pharmacology and Physiology, Chulalongkorn University, Bangkok, Thailand.

Rattana Saetung (R)

Faculty of Pharmaceutical Sciences, Department of Pharmacology and Physiology, Chulalongkorn University, Bangkok, Thailand.

Varalee Yodsurang (V)

Faculty of Pharmaceutical Sciences, Department of Pharmacology and Physiology, Chulalongkorn University, Bangkok, Thailand.

Chatchai Chaotham (C)

Faculty of Pharmaceutical Sciences, Department of Biochemistry and Microbiology, Chulalongkorn University, Bangkok, Thailand.

Koramit Suppipat (K)

Faculty of Medicine, Department of Research Affair, Chulalongkorn University, Bangkok, Thailand.
Cellular Immunotherapy Research Unit, Chulalongkorn University, Bangkok, Thailand.

Pithi Chanvorachote (P)

Faculty of Pharmaceutical Sciences, Department of Pharmacology and Physiology, Chulalongkorn University, Bangkok, Thailand.

Supannikar Tawinwung (S)

Faculty of Pharmaceutical Sciences, Department of Pharmacology and Physiology, Chulalongkorn University, Bangkok, Thailand.
Cellular Immunotherapy Research Unit, Chulalongkorn University, Bangkok, Thailand.

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