<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>24(1)</volume><submitter>Guohui T</submitter><pubmed_abstract>Exosomes are key mediators of communication between tumor cells and the tumor microenvironment(TME); however, the mechanisms underlying exosome-mediated crosstalk between tumor cells and macrophages remain largely unclear. This study investigated the effect of exosomal RAB10 on macrophage polarization and tumor growth. Mechanistically, RAB10 delivered by breast cancer cells binds to the interferon receptor IFNAR1 and inhibits JAK1/STAT1 pathway phosphorylation, thereby impeding M1 polarization and promoting M2 polarization. RAB10 expression was significantly upregulated in drug-resistant breast cancer cells and was correlated with poor patient prognosis. In vitro assays confirmed that RAB10 enhances cancer cell proliferation. In vivo knockdown of RAB10 suppressed tumor growth and reduced t</pubmed_abstract><journal>Cell communication and signaling : CCS</journal><pagination>123</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12918282</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Exosome RAB10 inhibits JAK1/STAT1 to hinder macrophage M1 polarization and promote tumor immune escape.</pubmed_title><pmcid>PMC12918282</pmcid><pubmed_authors>Wenrui W</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Bo P</pubmed_authors><pubmed_authors>Qiong W</pubmed_authors><pubmed_authors>Ruonan L</pubmed_authors><pubmed_authors>Ruorong R</pubmed_authors><pubmed_authors>Chengle Z</pubmed_authors><pubmed_authors>Qingling Y</pubmed_authors><pubmed_authors>Guohui T</pubmed_authors><pubmed_authors>Xu S</pubmed_authors><pubmed_authors>Changjie C</pubmed_authors><pubmed_authors>Cai H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Exosome RAB10 inhibits JAK1/STAT1 to hinder macrophage M1 polarization and promote tumor immune escape.</name><description>Exosomes are key mediators of communication between tumor cells and the tumor microenvironment(TME); however, the mechanisms underlying exosome-mediated crosstalk between tumor cells and macrophages remain largely unclear. This study investigated the effect of exosomal RAB10 on macrophage polarization and tumor growth. Mechanistically, RAB10 delivered by breast cancer cells binds to the interferon receptor IFNAR1 and inhibits JAK1/STAT1 pathway phosphorylation, thereby impeding M1 polarization and promoting M2 polarization. RAB10 expression was significantly upregulated in drug-resistant breast cancer cells and was correlated with poor patient prognosis. In vitro assays confirmed that RAB10 enhances cancer cell proliferation. In vivo knockdown of RAB10 suppressed tumor growth and reduced t</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Jan</publication><modification>2026-07-16T07:53:03.742Z</modification><creation>2026-07-09T10:46:20.66Z</creation></dates><accession>S-EPMC12918282</accession><cross_references><pubmed>41588435</pubmed><doi>10.1186/s12964-026-02681-x</doi></cross_references></HashMap>