Aspirin inhibit platelet‑induced epithelial‑to-mesenchymal transition of circulating tumor cells (Review)

Lou,Xiao‑Liang; Deng,Jun; Deng,Huan; Ting,Yuan; Zhou,Lv; Liu,Yan‑Hua; Hu,Jin‑Ping; Huang,Xiao‑Feng; Qi,Xiao‑Qing

doi:10.3892/br.2014.242

Aspirin inhibit platelet‑induced epithelial‑to-mesenchymal transition of circulating tumor cells (Review)

Authors:
- Xiao‑Liang Lou
- Jun Deng
- Huan Deng
- Yuan Ting
- Lv Zhou
- Yan‑Hua Liu
- Jin‑Ping Hu
- Xiao‑Feng Huang
- Xiao‑Qing Qi
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Affiliations: Department of Neurology, The Fourth Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330003, P.R. China, Emergency Department, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China, Department of Pathology, The Fourth Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330003, P.R. China
Published online on: February 27, 2014 https://doi.org/10.3892/br.2014.242
Pages: 331-334

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Abstract

Metastasis, a cascade of events beginning with epithelial‑to‑mesenchymal transition (EMT), is the main cause of cancer‑related mortality. EMT endows circulating cancer cells (CTCs) with invasive and anti‑apoptotic properties. These transitioning cells leave the primary tumor site and travel through the circulation to populate remote organs, even prior to the onset of clinical symptoms. During this journey, CTCs activate platelets, which in turn secrete α‑granules. These α‑granules contain high levels of transforming growth factor‑β (TGF‑β) and platelet‑derived growth factor (PDGF), both considered to be powerful activators of EMT. Recently, regular aspirin use was associated with a reduced risk of cancer metastasis. However, the molecular mechanism underlying the chemotherapeutic effects of aspirin on metastasis has not been fully elucidated. As platelets lack a nucleus, regular aspirin use may exert long‑lasting effects on irreversible inhibition of cyclooxygenase (COX)‑1 and, subsequently, the secretion of α‑granules, which contributes to the maintenance of the EMT state of CTCs. Thus, we hypothesized that the inhibition of platelet‑induced EMT of CTCs through the COX‑1 signaling pathway may contribute to the intriguing antimetastatic potential of aspirin.

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