The aspirin metabolite, salicylate, inhibits 7,12-dimethylbenz[a]anthracene-DNA adduct formation in breast cancer cells

  • Authors:
    • Giuliana Abbadessa
    • Angela Spaccamiglio
    • Maria Luisa Sartori
    • Carlo Nebbia
    • Mauro Dacasto
    • Francesco Di Carlo
    • Silvia Racca
  • View Affiliations

  • Published online on: May 1, 2006     https://doi.org/10.3892/ijo.28.5.1131
  • Pages: 1131-1140
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Abstract

There is evidence that aspirin and other non-steroidal anti-inflammatory drugs may be protective agents against cancer in the gastrointestinal tract. These effects are particularly well documented for the colon and rectum. Some epidemiological and experimental studies have suggested that aspirin could also be a chemopreventive agent against breast cancer. We investigated the effects of the aspirin metabolite, salicylate (SA), on 7,12-dimethylbenz[a]anthracene (DMBA)-DNA adduct formation as well as on the expression of the enzymes involved in the carcinogen bioactivation pathway, in particular cytochrome P450 1A (CYP1A) and cyclooxygenases (COX-1 and COX-2). The effects of the test drug were examined in both the human mammary carcinoma cell line, MCF-7, and mammary cells derived from DMBA-induced rat mammary tumours (RMTCs). In this study, we also reported the effects of SA on cell growth and viability in breast cancer cells (BCCs). The results demonstrated that DMBA-DNA adduct formation in both cancer cell lines was inhibited by SA at concentrations of ≥ 2.5 mM. CYP1A was undetectable in RMTCs while CYP1A induction by β-naphthoflavone in MCF-7 cells was significantly inhibited by SA in a concentration-dependent manner. Aspirin did not affect COX-1 expression in either of the BCCs. COX-2 was not detected in MCF-7 cells, but its expression in RMTCs was inhibited by SA treatment, which also significantly reduced BCC growth, but failed to cause cell death by necrosis or apoptosis. These data suggest that inhibition of DMBA-DNA adduct formation may contribute to aspirin breast cancer chemopreventive action and indicate that this drug can act in the first stage of carcinogenesis.

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May 2006
Volume 28 Issue 5

Print ISSN: 1019-6439
Online ISSN:1791-2423

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APA
Abbadessa, G., Spaccamiglio, A., Sartori, M.L., Nebbia, C., Dacasto, M., Di Carlo, F., & Racca, S. (2006). The aspirin metabolite, salicylate, inhibits 7,12-dimethylbenz[a]anthracene-DNA adduct formation in breast cancer cells. International Journal of Oncology, 28, 1131-1140. https://doi.org/10.3892/ijo.28.5.1131
MLA
Abbadessa, G., Spaccamiglio, A., Sartori, M. L., Nebbia, C., Dacasto, M., Di Carlo, F., Racca, S."The aspirin metabolite, salicylate, inhibits 7,12-dimethylbenz[a]anthracene-DNA adduct formation in breast cancer cells". International Journal of Oncology 28.5 (2006): 1131-1140.
Chicago
Abbadessa, G., Spaccamiglio, A., Sartori, M. L., Nebbia, C., Dacasto, M., Di Carlo, F., Racca, S."The aspirin metabolite, salicylate, inhibits 7,12-dimethylbenz[a]anthracene-DNA adduct formation in breast cancer cells". International Journal of Oncology 28, no. 5 (2006): 1131-1140. https://doi.org/10.3892/ijo.28.5.1131