Galangin, a
flavonoid isolated from the rhizome of Alpinia officinarum (Hance), exerts anticancer activities against many
cancer cells such as
liver cancer,
breast cancer,
lung cancer and
esophageal cancer. However, the effect, as well as the underlying molecular mechanism of
galangin on
gastric cancer remains to be elucidated. In the present study,
galangin inhibited cell viability of MGC 803 cells but not normal gastric mucosal epithelial GES-1 cells. It suppressed cell proliferation accompanied by reduced Ki67 and
PCNA expression, promoted apoptosis shown by decreased Bcl-2 and elevated cleaved
caspase-3 and cleaved PARP. And,
galangin significantly inactivated JAK2/STAT3 pathway. When STAT3 was overexpressed, the proliferation inhibition and apoptosis promotion induced by
galangin were abrogated. Meanwhile,
galangin increased ROS accumulation, and reduced Nrf2 and NQO-1, but elevated HO-1 in MGC 803 cells. NAC, a ROS scavenger, rescued ROS over-accumulation and proliferation inhibition of
galangin. STAT3 overexpression also counteracted excessive ROS accumulation induced by
galangin. Consistent with the in vitro experiments, in nude mice exnografted with MGC 803 cells,
galangin inhibited
tumor growth and reversed the abnormally expressed
proteins, such as p-JAK2, p-STAT3, Bcl-2, cleaved
caspase-3, cleaved PARP, and Ki67. Taken together,
galangin was suggested to inhibit the growth of MGC 803 cells through inducing apoptosis and decreasing cell proliferation, which might be mediated by modulating STAT3/ROS axis. Our findings implicate a potential application of
galangin for
gastric cancer therapy possibly with low toxicity.