ArticleMedComm2025
Glycoprotein Ibα-Dependent Platelet Activation is Essential for Tumor Cell-Platelet Interaction and Experimental Metastasis.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The trial behind it
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Who cites it
3 citing papers in PubMed.
- Platelet-derived mitochondrial transfer in cancer metastasis: mechanisms, functional consequences, and translational opportunities.Clinical & experimental metastasis · 2026Review
- Platelets as localized conduits of TGF-β1 in the tumor microenvironment: implications for cancer progression and therapy.Human cell · 2026Review
- Review
Corrections and comments
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Authors and funding
17 authors.
Funding
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Abstract
Metastasis is the main cause of cancer-related deaths and the biggest challenge in improving cancer prognosis. Platelet-tumor cell aggregates are a prerequisite for hematogenous metastasis. However, the internal relation and molecular mechanism of platelets and their receptor glycoprotein (GP) Ibα in platelet-tumor cell interaction and metastasis remain elusive. Here, we find that in the absence of the full-length GPIbα or its cytoplasmic tail, platelets maintain a more resting state and exhibit reduced tumor cell-induced platelet activation. The deficiency of the cytoplasmic tail of GPIbα inhibits tumor cell-platelet interaction, platelet-induced tumor cell migration and invasion, and metastasis. Using a state-of-the-art spinning disk intravital microscopy, we observe a rapid accumulation of platelets on tumor cells, forming numerous tumor cell-platelet aggregates in vivo. We also find that the cytoplasmic tail of GPIbα regulates the tumor cell-induced platelet protein kinase C-α (PKCα) activation, and both the pharmacological inhibition and genetic ablation of platelet PKCα attenuate tumor cell-induced platelet activation, tumor cell-platelet interaction, tumor cell migration and invasion, and metastasis. Overall, our findings reveal for the first time that GPIbα promotes experimental metastasis through its cytoplasmic tail-regulated platelet activation, and suggest a potential target to regulate tumor hematogenous metastasis.
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