Journal Article

NO-donating aspirin inhibits the activation of NF-κB in human cancer cell lines and <i>Min</i> mice

Jennie L. Williams, Ping Ji, Nengtai Ouyang, Xiaoping Liu and Basil Rigas

in Carcinogenesis

Volume 29, issue 2, pages 390-397
Published in print February 2008 | ISSN: 0143-3334
Published online January 2008 | e-ISSN: 1460-2180 | DOI:
NO-donating aspirin inhibits the activation of NF-κB in human cancer cell lines and Min mice

More Like This

Show all results sharing this subject:

  • Clinical Cytogenetics and Molecular Genetics


Show Summary Details


Nitric oxide-donating aspirin (NO-ASA) is a promising agent for the control of cancer, whose mechanism of action remains unclear. NF-κB is an important signaling molecule in the pathogenesis of cancer. We studied in several human colon (HT-29, HCT-15, LoVo, HCT116 and SW-480), pancreatic (BxPC-3, MIA PaCa-2) and breast (MDA-MB-231 and MCF-7) cancer cell lines, the effect of NO-ASA on NF-κB activation, determined by electrophoretic mobility shift assays, immunofluorescence and western blot analyses of nuclear proteins. NO-ASA inhibited NF-κB activation, as early as 30 min and with IC50s ranging between 0.83 and 64 μM. Such inhibition was also observed at NO-ASA concentrations that had an insignificant or marginal effect on cell growth. The effect of NO-ASA on NF-κB binding to DNA was significantly correlated with its effect on cell growth (P < 0.05) indicating that the growth inhibitory effect of NO-ASA may be mediated by its effect on NF-κB. Compared with control, NO-ASA decreased NF-κB activation in intestinal epithelial cells of APCmin+/− mice by 38.4% (P < 0.01). Western blot and immunofluorescence analyses revealed that the nuclear levels of the p50 and p65 NF-κB subunits were virtually unaffected, suggesting an inhibitory mechanism different from suppressed subunit translocation into the nucleus. Inhibition of NF-κB activation by NO-ASA may account, at least in part, for its chemopreventive efficacy.

Journal Article.  5430 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.