The most common cause of colorectal cancer-related mortality is metastasis. Approximately 60% of colorectal cancer patients are expected to develop metastases. The egress of micrometastases from the vascular system is facilitated by the formation of complexes between platelets and tumour cells. However, it is not clear the molecular mechanisms of platelet-tumor cell interaction. Pinpointing the molecules responsible for platelet-tumor cell interaction was largely hampered by the existence of adhesion molecule variants on tumor cells, which differ in adhesion outfits and thus enable tumor cells with distinct metastatic activities. Lipid microdomains on the cellular membrane convene adhesion molecules and intracellular signals and are essential for tumor cell adhesion, growth, invasion, and metastasis. We thus tried to identify the adhesion and signaling molecules located on lipid rafts by proteomics and confirm their roles in platelet-tumor cell adhesion by functional adhesion assays. The present study showed that lipid rafts were essential in mediating platelet-tumor cell adhesion. Proteomic analysis of isolated tumor cell lipid rafts indicates that integrin?4 may be a new important adhesion molecules in bridging platelet and colorectal cancer cell. Functional adhesion studies performed on a parallel-plate flow chamber further suggested that platelet GPIIb/IIIa is a major counterpart molecule for platelet-tumor cell adhesion. The present study may provide a new approach for investigating platelet-tumor cell interaction and help in the prevention and therapy of colorectal cancer metastasis.
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Source: http://www.res-medical.com/oncology/62355
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