Abstract
Blood platelets foster carcinogenesis. We found that platelets are accumulated in human tumors. P-selectin deficiency and soluble P-selectin abolish platelet deposition within tumors, decreasing secretion of vascular endothelial growth factor and angiogenesis, thereby suppressing tumor growth. Binding of the P-selectin cytoplasmic tail to talin1 triggers the talin1 N-terminal head to interact with the β3 cytoplasmic tail. This activates αIIbβ3 and recruits platelets into tumors. Platelet infiltration into solid tumors occurs through a P-selectin-dependent mechanism.
Keywords:
P-selectin; platelets; talin1; tumor growth; αIIbβ3.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blood Platelets / metabolism*
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Cell Proliferation*
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Female
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Humans
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Insulinoma / blood
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Insulinoma / genetics
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Insulinoma / metabolism*
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Insulinoma / pathology
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Melanoma, Experimental / blood
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Melanoma, Experimental / metabolism*
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Melanoma, Experimental / pathology
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Mice, Inbred C57BL
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Mice, Knockout
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P-Selectin / blood
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P-Selectin / genetics
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P-Selectin / metabolism*
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Pancreatic Neoplasms / blood
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Pancreatic Neoplasms / genetics
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Pancreatic Neoplasms / metabolism*
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Pancreatic Neoplasms / pathology
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Platelet Adhesiveness*
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Platelet Glycoprotein GPIIb-IIIa Complex / metabolism
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Protein Binding
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Signal Transduction
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Talin
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Time Factors
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Tumor Burden
Substances
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P-Selectin
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Platelet Glycoprotein GPIIb-IIIa Complex
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SELP protein, human
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Talin
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Tln1 protein, mouse