The role of mucin-educated platelet activation in tumor invasiveness: An unfolding concern in the realm of cancer biology.

Metastasis is a complex and well-coordinated phenotypic transformation of cancer cells governed by aberrant genetic and molecular pathways. It has been approved as the most consistent cause of cancer death. With emerging insight into the genomics, transcriptomics and proteomics, progress has been made and reasonably large number of molecular pathways of metastasis has been forwarded, but our understanding of precise underlying molecular mechanisms remains largely scarce. It has been well-known for around a decade and more that platelets are intriguingly contributing to the cancer metastasis. However, it is only recently that cancer cells can activate platelets have started to become apparent. Surprisingly, platelets in response to cancer cell activation, supported by research observations, allow cancer cells to escape immune removal, prolong survival in vascular compartment, increased cellular adhesion and develop new cellular niches which eventually help to favor cancer metastasis. Although a widely acknowledged plausible explanation that cancer cells activate platelets to facilitate in their distant spread, the description of this remains to be confirmed. In recent years, mucins, heavily glycosylated peptide structure, have been introduced to be released by several types of cancer cells. They account for poor prognosis in wide array of malignancies, because of their significant ability to induce metastatic process. The mechanism responsible for their increased metastatic propensity remains uncharacterized, but recent work suggested the role of cancer expressed mucins in initiating platelet thrombus. The association of cancer yield mucins, platelets and metastasis therefore suggests a pressing need to explore novel molecular mechanisms and therapeutic targets thereafter.