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The induction of a mesenchymal phenotype by platelet cloaking of cancer cells is a universal phenomenon

Authors
  • Spillane, Cathy D.
  • Cooke, Niamh M.
  • Ward, Mark P.
  • Kenny, Dermot
  • Blackshields, Gordon
  • Kelly, Tanya
  • Bates, Mark
  • Huang, Yanmei
  • Martin, Cara
  • Skehan, Sinead
  • Canney, Aoife
  • Gallagher, Michael
  • Smyth, Paul
  • Brady, Nathan
  • Clarke, Andres
  • Mohamed, Bashir
  • Norris, Lucy
  • Brooks, Doug A.
  • Brooks, Robert D.
  • Heatlie, Jessica K.
  • And 6 more
Type
Published Article
Journal
Translational Oncology
Publisher
Neoplasia Press
Publication Date
Sep 27, 2021
Volume
14
Issue
12
Identifiers
DOI: 10.1016/j.tranon.2021.101229
PMID: 34592589
PMCID: PMC8488306
Source
PubMed Central
Keywords
Disciplines
  • Original Research
License
Unknown

Abstract

Tumour metastasis accounts for over 90% of cancer related deaths. The platelet is a key blood component, which facilitates efficient metastasis. This study aimed to understand the molecular mechanisms involved in tumour-platelet cell interactions. The interaction between cancer cells and platelets was examined in 15 epithelial cell lines, representing 7 cancer types. Gene expression analysis of EMT-associated and cancer stemness genes was performed by RT-PCR. Whole transcriptome analysis (WTA) was performed using Affymetrix 2.0ST arrays on a platelet co-cultured ovarian model. Platelet adhesion and activation occurred across all tumour types. WTA identified increases in cellular movement, migration, invasion, adhesion, development, differentiation and inflammation genes and decreases in processes associated with cell death and survival following platelet interaction. Increased invasive capacity was also observed in a subset of cell lines. A cross-comparison with a platelet co-cultured mouse model identified 5 common altered genes; PAI-1, PLEK2, CD73, TNC, and SDPR. Platelet cancer cell interactions are a key factor in driving the pro-metastatic phenotype and appear to be mediated by 5 key genes which have established roles in metastasis. Targeting these metastasis mediators could improve cancer patient outcomes.

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