Volume 7, Number 4, December 2017
|Number of page(s)||3|
|Published online||13 November 2017|
The role of mucin-educated platelet activation in tumor invasiveness: An unfolding concern in the realm of cancer biology
Senior Research Assistant, Maternal and Fetal Medicine, Department of Obstetrics & Gynaecology, The Aga Khan University Hospital, Karachi 74800, Pakistan
2 Pharm. D Student, Department of Pharmacy, Jinnah University for Women, Karachi 74600, Pakistan
* Corresponding author. Flat # B-107, Al-Noor Co-operative Housing Society, Block-K, North Nazimabad, Karachi 74700, Pakistan. E-mail address: email@example.com (A. S. Ali).
Received: 8 May 2017
Accepted: 11 July 2017
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.
Key words: Mucins / Platelets / Cancer / Metastasis
© Author(s) 2017. This article is published with open access by China Medical University
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