ArticleBreast cancer research : BCR2025
Tumor-educated-platelets interact with breast cancer-stem-cells via P-selectin-PSGL1 and ensure stemness and metastasis through WNT-β-catenin-VEGF-VEGFR2 intra-cellular signaling: therapeutic modulation by aspirin.
Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- NNMT-associated metabolic-thromboinflammatory-immune co-activation in heterogeneous CTC clusters: a hypothesis-generating computational framework".BMC cancer · 2026Article
- Enhancing EGFR Inhibition: Monensin and Erlotinib Synergize to Eliminate Cancer Stem Cells in Canine Mammary Tumours.Veterinary and comparative oncology · 2026Article
- SP1-IKBIP axis promotes the proliferation and invasion of glioma with Wnt/β-catenin associated epithelial-mesenchymal transition.American journal of cancer research · 2026Article
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22 authors.
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Abstract
backgroundProtagonistic role of platelets promote capillary infiltration of tumors for distant metastasis along with immunosurveillance. Despite existing reports highlighting role of platelets in tumorigenesis, its impact on breast cancer stem cells (BCSCs) remain underexplored. Our first ever report on murine and human system, accentuate that, tumor educated platelets (TEPs) of luminal A and TNBC subtypes are distinct from healthy counterparts, collaborating with BCSCs to generate sub-variants that elevate tumor aggressiveness.
methodsImpact of TEPs on BCSCs was evaluated from primary breast tumor and blood samples of luminal A/TNBC patients along with EC/4T1 murine breast tumor models and MCF-7/MDA-MB-231 cell lines. For downstream assays, TEPs were co-cultured with breast tumor samples or cell lines, followed by magnetic sorting of lin
resultsTEPs have elevated expression of P-selectin and interacts with BCSCs via P-selectin and PSGL1 on BCSCs surface. Treatment with aspirin had restorative impact on P-selectin level, converting TEPs from active to resting platelet (RP) state. Under TEPs influence, BCSCs were tumorigenic, clonogenic, multidrug resistant, invasive with numerous invadopodia and remained skewed towards mesenchymal phenotype. Administration of RP reduced TEP associated BCSC virulence both in-vivo and in-vitro. P-selectin-PSGL1 interaction results in binding of WNT to FRIZZLED followed by stabilization and nuclear translocation of β-catenin. Nuclear β-catenin promotes stemness-EMT (Epithelial to mesenchymal transition)-metastasis, along with stimulation of autocrine VEGF-VEGFR2 cascade. Inhibition of WNT and VEGFR2 by RNAi confirmed the critical role of this axis in regulating TEP's influence on BCSCs.
conclusionThese insights into TEP-BCSC interplay, acknowledges TEPs, as-well-as unveils novel receptor-ligand signaling cascade between TEPs and BCSCs, that could be a beneficial therapeutic strategy to target cancer metastasis.
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