Modulations of benzo[a]pyrene-induced DNA adduct, cyclin D1 and PCNA in oral tissue by 1,4-phenylenebis(methylene)selenocyanate.
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.
Chen
Kun-Ming
KM
Department of Biochemistry and Molecular Biology, Penn State College of Medicine, Hershey, PA 17033, USA.
Sacks
Peter G
PG
Spratt
Thomas E
TE
Lin
Jyh-Ming
JM
Boyiri
Telih
T
Schwartz
Joel
J
Richie
John P
JP
Calcagnotto
Ana
A
Das
Arunangshu
A
Bortner
James
J
Zhao
Zonglin
Z
Amin
Shantu
S
Guttenplan
Joseph
J
El-Bayoumy
Karam
K