Modulations of benzo[a]pyrene-induced DNA adduct, cyclin D1 and PCNA in oral tissue by 1,4-phenylenebis(methylene)selenocyanate

Kun Ming Chen, Peter G. Sacks, Thomas E. Spratt, Jyh Ming Lin, Telih Boyiri, Joel Schwartz, John P. Richie, Ana Calcagnotto, Arunangshu Das, James Bortner, Zonglin Zhao, Shantu Amin, Joseph Guttenplan, Karam El-Bayoumy

Research output: Contribution to journalArticlepeer-review


Tobacco smoking is an important cause of human oral squamous cell carcinoma (SCC). Tobacco smoke contains multiple carcinogens include polycyclic aromatic hydrocarbons typified by benzo[a]pyrene (B[a]P). Surgery is the conventional treatment approach for SCC, but it remains imperfect. However, chemoprevention is a plausible strategy and we had previously demonstrated that 1,4-phenylenebis(methylene)selenocyanate (p-XSC) significantly inhibited tongue tumors-induced by the synthetic 4-nitroquinoline-N-oxide (not present in tobacco smoke). In this study, we demonstrated that p-XSC is capable of inhibiting B[a]P-DNA adduct formation, cell proliferation, cyclin D1 expression in human oral cells in vitro. In addition, we showed that dietary p-XSC inhibits B[a]P-DNA adduct formation, cell proliferation and cyclin D1 protein expression in the mouse tongue in vivo. The results of this study are encouraging to further evaluate the chemopreventive efficacy of p-XSC initially against B[a]P-induced tongue tumors in mice and ultimately in the clinic.

Original languageEnglish (US)
Pages (from-to)151-155
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - May 22 2009


  • B[a]P
  • Chemoprevention
  • Selenium
  • p-XSC

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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