ArticleScientific reports2026
M2 macrophage-derived extracellular vesicles induce EMT-like transcriptional reprogramming in colorectal cancer cells via upregulation of FAM83A.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Unlocking the stability and storage conditions of plant-derived nanovesicles through metabolomic and lipidomic profiling.Scientific reports · 2026Article
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3 authors.
Funding
Abstract
In the complex landscape of cancer progression, the immune system shapes crucial interactions between tumor and immune cells. Understanding this dialogue is essential for elucidating how immune-derived cues trigger epithelial-mesenchymal transition (EMT)-like transcriptional changes, a fundamental process that drives tumor cell plasticity and facilitates aggressive phenotypes. Here, we investigated the crosstalk between M2 macrophages and colon cancer cells (HT-29) during the post-tumorigenic phase, focusing on exosome-mediated regulation of EMT, a critical pathway controlling tumor cell phenotypic and transcriptional dynamics. Co-culture experiments revealed that M2 macrophage-derived exosomes (M2-Exo) induced profound transcriptional changes, with downregulation of epithelial markers and increased expression of mesenchymal genes. Importantly, EMT induction was markedly stronger following M2-Exo treatment than in the co-culture setting, suggesting that while soluble mediators play a contributory role, EMT is predominantly and directly driven by exosome-mediated signaling. Transcriptomic profiling identified FAM83A as a key upregulated gene in M2-Exo-treated HT-29 cells. Functional analyses demonstrated that FAM83A promoted EMT by modulating regulators associated with decreased E-Cadherin and increased N-Cadherin, MMP2, and MMP9 expression. Importantly, siRNA-mediated silencing of FAM83A abolished its overexpression and inhibited EMT activation, confirming its essential role in M2-Exo-induced programming of EMT. Collectively, these findings highlight exosome-mediated immune-tumor interactions as critical drivers of EMT and the progression toward an invasive, mesenchymal-like phenotype.
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