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This study aims to investigate whether delivering si\u2010Forkhead Box M1 (FOXM1) efficiently into tumour cells via lipid nanoparticles (LNPs) can silence\n                      <jats:italic>FOXM1<\/jats:italic>\n                      expression, up\u2010regulate Kruppel\u2010like factor 15 (KLF15) and thereby modulate TAM polarization to enhance the antitumor immune response against breast cancer.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>Transcriptomic data from TCGA and GEO were analysed using Weighted Gene Co\u2010expression Network Analysis (WGCNA) and CIBERSORT for immune infiltration. Cell culture, gene expression, and functional assays assessed the impact of FOXM1 silencing on TAM polarization and breast cancer cell behaviour. si\u2010FOXM1\u2010loaded LNPs were characterized and evaluated both in vitro and in vivo xenograft models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      The study identified\n                      <jats:italic>KLF15<\/jats:italic>\n                      as a key player associated with breast cancer prognosis and showed that\n                      <jats:italic>FOXM1<\/jats:italic>\n                      silencing promoted\n                      <jats:italic>KLF15<\/jats:italic>\n                      expression, leading to reduced M2 macrophage infiltration and inhibited breast cancer progression. LNPs loaded with si\u2010FOXM1 efficiently reprogrammed TAMs to the M1 phenotype, inhibiting breast cancer cell proliferation and invasion.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      LNPs loaded with si\u2010FOXM1 act on tumour cells to silence\n                      <jats:italic>FOXM1<\/jats:italic>\n                      expression and up\u2010regulate\n                      <jats:italic>KLF15<\/jats:italic>\n                      , thereby promoting the reprogramming of tumour\u2010associated macrophages towards the M1 phenotype within the tumour microenvironment. This process effectively inhibits breast cancer progression and enhances the antitumor efficacy of immune checkpoint inhibitors against breast cancer cells.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70330","type":"journal-article","created":{"date-parts":[[2026,2,22]],"date-time":"2026-02-22T22:50:40Z","timestamp":1771800640000},"page":"3049-3073","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Reprogramming tumour\u2010associated macrophages in breast cancer via si\u2010FOXM1\u2010loaded lipid nanoparticles enhances immune checkpoint inhibitor efficacy"],"prefix":"10.1111","volume":"183","author":[{"given":"Yali","family":"Gao","sequence":"first","affiliation":[{"name":"School of Clinical Medicine Ningxia Medical University  Yinchuan P. R. 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