Aspirin inhibits cancer stem cells properties and growth of glioblastoma multiforme through Rb1 pathway modulation

Giacomo Pozzoli, Hany E Marei, Asma Althani, Alma Boninsegna, Patrizia Casalbore, Lionel N J L Marlier, Giulia Lanzilli, Manuela Zonfrillo, Giovanna Petrucci, Bianca Rocca, Pierluigi Navarra, Alessandro Sgambato, Carlo Cenciarelli

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
JournalJournal of Cellular Physiology
DOIs
Publication statusE-pub ahead of print - Jan 30 2019

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