Apicidin, a
cyclic peptide histone deacetylase (
HDAC) inhibitor, has been demonstrated to exhibit antitumor activity in a number of human
cancer types. The present study examined the antitumor activity of
apicidin in murine
oral squamous cell carcinoma (OSCC) cells. Inhibition of cell proliferation and the expression of selective HDACs were determined in
apicidin-treated AT-84 murine OSCC cells. A C3H mouse model with
subcutaneous injection of AT-84 cells was used to assess the in vivo effect of
apicidin on
tumor growth.
Apicidin-induced cell growth inhibition and selectively reduced HDAC8 expression in AT-84 cells. Induction of apoptosis and autophagy was observed in
apicidin-treated AT-84 cells.
Apicidin notably inhibited
tumor growth by up to 46% relative to the control group at the end of a 14-day period in a murine
tumor model. The immunohistochemistry results in
tumor tissues indicated that
apicidin inhibited cell proliferation and induced apoptosis and autophagy in AT-84 cell-derived
tumor tissues. Overexpression of HDAC8 was observed in the nucleus and cytoplasm in
tumor tissues and
apicidin significantly inhibited the level of HDAC8 expression, compared with the vehicle group. These results indicated that
apicidin inhibited cell proliferation through HDAC8 inhibition in murine OSCC cells in vitro and in vivo. The present study indicated that
apicidin may be an effective therapeutic agent for OSCC.