Gentian violet induces wtp53 transactivation in cancer cells

Alessia Garufi, Valerio D'Orazi, Jack L. Arbiser, Gabriella D'Orazi

Research output: Contribution to journalArticlepeer-review


Recent studies suggest that gentian violet (GV) may have anticancer activity by inhibiting for instance NADPH oxidases (Nox genes) whose overexpression is linked to tumor progression. Nox1 overexpression has been shown to inhibit transcriptional activity of the oncosuppressor p53, impairing tumor cell response to anticancer drugs. The tumor suppressor p53 is a transcription factor that, upon cellular stress, is activated to induce target genes involved in tumor cell growth inhibition and apoptosis. Thus, its activation is important for efficient tumor eradication. In this study, we examined the effect of GV on wild-type (wt) p53 activity in cancer cells. We found that GV was able to overcome the inhibitory effect of the NADPH oxidase Nox1 on p53 transcriptional activity. For the first time we show that GV was able to directly induce p53/DNA binding and transcriptional activity. In vitro, GV markedly induced cancer cell death and apoptotic marker PARP cleavage in wtp53-carrying cells. GV-induced cell death was partly inhibited in cells deprived of p53, suggesting that the anticancer activity of GV may partly depend on p53 activation. GV is US Food and Drug Administration approved for human use and may, therefore, have therapeutic potential in the management of cancer through p53 activation.

Original languageEnglish
Pages (from-to)1084-1090
Number of pages7
JournalInternational Journal of Oncology
Issue number4
Publication statusPublished - Apr 2014


  • Cancer therapy
  • DNA binding
  • Gene expression
  • Gentian violet
  • NADPH oxidase 1
  • p53 transcriptional activity

ASJC Scopus subject areas

  • Cancer Research
  • Oncology
  • Medicine(all)


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