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

Giacomo Pozzoli*, Giovanna Petrucci, Pierluigi Navarra, Hany E. Marei, Carlo Cenciarelli

*Autore corrispondente per questo lavoro

Risultato della ricerca: Contributo in rivistaArticolo in rivista

3 Citazioni (Scopus)

Abstract

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.
Lingua originaleEnglish
pagine (da-a)7078-7087
Numero di pagine10
RivistaJournal of Cellular and Molecular Medicine
Volume2019
DOI
Stato di pubblicazionePubblicato - 2019

Keywords

  • aspirin
  • neuroblastoma

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