In:
Journal of Cellular Physiology, Wiley, Vol. 234, No. 9 ( 2019-09), p. 15459-15471
Kurzfassung:
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 E 2 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.
Materialart:
Online-Ressource
ISSN:
0021-9541
,
1097-4652
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2019
ZDB Id:
1478143-8
SSG:
12
