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Tumor-associated macrophages (TAMs), abundant in BC TME, mainly acquire an immunosuppressive M2-like phenotype able to fuel tumor progression, immune evasion, metastasis and therapy resistance through a dynamic crosstalk with cancer cells. MicroRNAs, transferred via extracellular vesicles and exploited by the tumor to mold an immunesuppressive niche, act as central mediators of this bidirectional communication: tumor-derived miRNAs can reprogram macrophages toward an M2-like functional program, and TAM-derived miRNAs in turn promote and sustain cancer cell progression. This miRNA-orchestrated plasticity highlights TAMs as key TME regulators. Clinically, miRNA modulation offers promising strategies for TAM reprogramming, alongside their utility as prognostic biomarkers. Integrating miRNA-targeted TME interventions with conventional therapies holds the potential to overcome resistance in high-TAM BC subtypes.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1792965","type":"journal-article","created":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T06:54:29Z","timestamp":1771397669000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["MiRNAs: a call to arms that shapes the plasticity of tumor associated macrophages in breast cancer"],"prefix":"10.3389","volume":"17","author":[{"given":"Valentina","family":"Fogazzi","sequence":"first","affiliation":[{"name":"Microenvironment and Biomarkers of Solid Tumors Unit, Department of Experimental Oncology, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano","place":["Milan, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giulia","family":"Cosentino","sequence":"additional","affiliation":[{"name":"Microenvironment and 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