<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>25(1)</volume><submitter>Duan X</submitter><pubmed_abstract>Cancer-associated fibroblasts (CAFs) can interact with macrophages in the tumor microenvironment by secreting extracellular vesicles (EVs), thereby affecting tumor progression. However, the mechanisms of CAF-secreted EVs in gastric cancer (GC) remain not well understood. Here, we investigated the effect of CAF-EVs on macrophage polarization in GC and the underlying mechanisms. Macrophage polarization was evaluated using flow cytometry and quantitative real-time polymerase chain reaction. GC cell proliferation was determined using cell counting kit-8, EdU, and colony formation assays. The molecular mechanism was explored using microarray analysis, dual-luciferase reporter assay, and RNA pull-down analysis. The results showed that CAFs secreted EVs that inhibit macrophage M1 polarization and</pubmed_abstract><journal>Cancer biology &amp; therapy</journal><pagination>2424490</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11542604</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Extracellular vesicle-packaged miR-4253 secreted by cancer-associated fibroblasts facilitates cell proliferation in gastric cancer by inducing macrophage M2 polarization.</pubmed_title><pmcid>PMC11542604</pmcid><pubmed_authors>Gan J</pubmed_authors><pubmed_authors>Duan X</pubmed_authors><pubmed_authors>Yu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Extracellular vesicle-packaged miR-4253 secreted by cancer-associated fibroblasts facilitates cell proliferation in gastric cancer by inducing macrophage M2 polarization.</name><description>Cancer-associated fibroblasts (CAFs) can interact with macrophages in the tumor microenvironment by secreting extracellular vesicles (EVs), thereby affecting tumor progression. However, the mechanisms of CAF-secreted EVs in gastric cancer (GC) remain not well understood. Here, we investigated the effect of CAF-EVs on macrophage polarization in GC and the underlying mechanisms. Macrophage polarization was evaluated using flow cytometry and quantitative real-time polymerase chain reaction. GC cell proliferation was determined using cell counting kit-8, EdU, and colony formation assays. The molecular mechanism was explored using microarray analysis, dual-luciferase reporter assay, and RNA pull-down analysis. The results showed that CAFs secreted EVs that inhibit macrophage M1 polarization and</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2025-04-04T14:56:59.815Z</modification><creation>2025-04-04T14:56:59.815Z</creation></dates><accession>S-EPMC11542604</accession><cross_references><pubmed>39505708</pubmed><doi>10.1080/15384047.2024.2424490</doi></cross_references></HashMap>