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J Cell Mol Med. 2019 Oct;23(10):7078-7087. doi: 10.1111/jcmm.14610. Epub 2019 Aug 20.

Aspirin inhibits proliferation and promotes differentiation of neuroblastoma cells via p21Waf1 protein up-regulation and Rb1 pathway modulation.

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Institute of Pharmacology, Università Cattolica del Sacro Cuore, Rome, Italy.
Pharmacology Unit, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Department of Cytology and Histology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, Egypt.
Institute of Translational Pharmacology (IFT), National Research Council (CNR), Rome, Italy.


Several clinical and experimental studies have demonstrated that regular use of aspirin (acetylsalicylic acid, ASA) correlates with a reduced risk of cancer and that the drug exerts direct anti-tumour effects. We have previously reported that ASA inhibits proliferation of human glioblastoma multiforme-derived cancer stem cells. In the present study, we analysed the effects of ASA on nervous system-derived cancer cells, using the SK-N-SH (N) human neuroblastoma cell line as an experimental model. ASA treatment of SK-N-SH (N) dramatically reduced cell proliferation and motility, and induced neuronal-like differentiation, indicated by the appearance of the neuronal differentiation marker tyrosine hydroxylase (TH) after 5 days. ASA did not affect cell viability, but caused a time-dependent accumulation of cells in the G0 /G1 phase of the cell cycle, with a concomitant decrease in the percentage of cells in the G2 phase. These effects appear to be mediated by a COX-independent mechanism involving an increase in p21Waf1 and underphosphorylated retinoblastoma (hypo-pRb1) protein levels. These findings may support a potential role of ASA as adjunctive therapeutic agent in the clinical management of neuroblastoma.


Rb1; acetylsalicylic acid; cell cycle; neuroblastoma; neuronal differentiation

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