ArticleCell communication and signaling : CCS2025
Bisecting GlcNAc modification of vesicular GAS6 regulates CAFs activation and breast cancer metastasis.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Small extracellular vesicles as system-level regulators and predictive biomarkers in breast cancer progression and chemoresistance.Frontiers in pharmacology · 2026Review
- Downregulation of MGAT3 Promotes Benzo[ACS omega · 2025Article
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Authors and funding
11 authors.
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Abstract
backgroundCancer-associated fibroblasts (CAFs) are a pivotal component of the tumor microenvironment (TME), playing key roles in tumor initiation, metastasis, and chemoresistance. While glycosylation is known to regulate various cellular processes, its impact on CAFs activation remains insufficiently explored.
methodsWe assessed the correlation between bisecting GlcNAc levels and CAFs markers (α-SMA, PDGFRA, PDGFRB) in breast cancer tissues. The effects of small extracellular vesicles (sEVs) derived from MDA-MB-231/OE
resultsWe found that low bisecting GlcNAc levels were associated with CAFs activation within the TME of breast cancer. Breast cancer-derived sEVs stimulated the conversion of normal fibroblasts to CAFs, with GAS6 in sEVs playing a key role by interacting with AXL receptors on fibroblasts. Introducing GAS6 into normal fibroblasts induced their conversion into CAFs, which enhanced breast cancer cell metastasis. Notably, GAS6 was decorated with bisecting GlcNAc, which promoted its degradation in donor cells, leading to reduced GAS6 levels in sEVs and attenuating GAS6-mediated CAFs activation.
conclusionTaken together, our findings provide new insights into the functional role of bisecting GlcNAc on GAS6-mediated CAFs activation in breast cancer.
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