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Cancer Metastasis Rev. 2017 Jun;36(2):289-303. doi: 10.1007/s10555-017-9675-z.

Beyond COX-1: the effects of aspirin on platelet biology and potential mechanisms of chemoprevention.

Author information

1
Department of Cancer Systems Imaging, Division of Diagnostic Imaging, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
2
Department of Gastrointestinal (GI) Medical Oncology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
3
Department of Epidemiology, Division of Cancer Prevention and Population Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
4
McGovern Medical School, Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX, USA.
5
Department of Systems Biology, Proteomics and Metabolomics Facility, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
6
Department of Clinical Cancer Prevention, Division of OVP, Cancer Prevention and Population Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
7
Department of Cancer Systems Imaging, Division of Diagnostic Imaging, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. smillward@mdanderson.or.

Abstract

After more than a century, aspirin remains one of the most commonly used drugs in western medicine. Although mainly used for its anti-thrombotic, anti-pyretic, and analgesic properties, a multitude of clinical studies have provided convincing evidence that regular, low-dose aspirin use dramatically lowers the risk of cancer. These observations coincide with recent studies showing a functional relationship between platelets and tumors, suggesting that aspirin's chemopreventive properties may result, in part, from direct modulation of platelet biology and biochemistry. Here, we present a review of the biochemistry and pharmacology of aspirin with particular emphasis on its cyclooxygenase-dependent and cyclooxygenase-independent effects in platelets. We also correlate the results of proteomic-based studies of aspirin acetylation in eukaryotic cells with recent developments in platelet proteomics to identify non-cyclooxygenase targets of aspirin-mediated acetylation in platelets that may play a role in its chemopreventive mechanism.

KEYWORDS:

Acetylome; Aspirin; Chemoprevention; Cyclooxygenase-1; Cyclooxygenase-2; Platelets

PMID:
28762014
PMCID:
PMC5557878
DOI:
10.1007/s10555-017-9675-z
[Indexed for MEDLINE]
Free PMC Article

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