Al's Comment:
Interesting experiment. Of course it is too early to tell if it will help people with a GBM, but something like this should be easy to pick up in our virtual trial. For those of you who are participating, and take aspirin on a regular basis, go back in and enter it!
Warning: Talk to your doctor before taking Aspirin. It can also increase the chances of bleeding. It might also help prevent blood clots - but this is a delicate balance.
Posted on: 02/13/2019
J Cell Physiol. 2019 Jan 30. doi: 10.1002/jcp.28194. [Epub ahead of print]
Aspirin inhibits cancer stem cells properties and growth of glioblastoma multiforme through Rb1 pathway modulation.
Pozzoli G1,2, Marei HE3, Althani A4, Boninsegna A5, Casalbore P6, Marlier LNJL7, Lanzilli G7, Zonfrillo M7, Petrucci G1, Rocca B1, Navarra P1,2, Sgambato A5, Cenciarelli C7.
Author information:
1. Institute of Pharmacology, Università Cattolica del Sacro Cuore, Rome, Italy.
2. Pharmacology Unit, Fondazione Policlinico A. Gemelli IRCCS, Rome, Italy.
3. Department of Cytology and Histology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, Egypt.
4. Biomedical Research Center, Qatar University, Doha, Qatar.
5. Institute of General Pathology, Università Cattolica del Sacro Cuore, Rome, Italy.
6. Department of Biomedical Sciences, Institute of Cell Biology and Neurobiology (IBCN), National Research Council (CNR), Rome, Italy.
7. Department of Biomedical Sciences, Institute of Translational Pharmacology (IFT), National Research Council (CNR), Rome, Italy.
Abstract
Several clinical studies indicated that the daily use of aspirin or acetylsalicylic acid reduces the cancer risk via cyclooxygenases (Cox-1 and Cox-2) inhibition. In addition, aspirin-induced Cox-dependent and -independent antitumor effects have also been described. Here we report, for the first time, that aspirin treatment of human glioblastoma cancer (GBM) stem cells, a small population responsible for tumor progression and recurrence, is associated with reduced cell proliferation and motility. Aspirin did not interfere with cell viability but induced cell-cycle arrest. Exogenous prostaglandin E2 significantly increased cell proliferation but did not abrogate the aspirin-mediated growth inhibition, suggesting a Cox-independent mechanism. These effects appear to be mediated by the increase of p21 waf1 and p27 Kip1 , associated with a reduction of Cyclin D1 and Rb1 protein phosphorylation, and involve the downregulation of key molecules responsible for tumor development, that is, Notch1, Sox2, Stat3, and Survivin. Our results support a possible role of aspirin as adjunctive therapy in the clinical management of GBM patients.
© 2019 Wiley Periodicals, Inc.
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