β-
asarone is the main active ingredient of the Chinese herb Rhizoma Acori Tatarinowii, which exhibits a wide range of
biological activities. It was confirmed to be an efficient
cytotoxic agent against gastroenteric
cancer cells. However, the exact mechanism of β-
asarone in
gastric cancer (GC) remains to be elucidated. The present study showed the inhibitory effect of β-
asarone on three types of different differentiation stage GC cell lines (MGC803, SGC7901, and MKN74) in a dose-dependent manner. Meanwhile, the synergistic sensitivity of β-
asarone and
cisplatin was confirmed by using the median-effect principle. Flow cytometry assay revealed that under both normoxia and CoCl2-induced
hypoxia conditions, β-
asarone can induce apoptosis of GC cells, which can block GC cells in the cell cycle G2/M phase, showing obvious subdiploid peak. Moreover, the activity of lactic
dehydrogenase (LDH), an
enzyme that plays an important role in the final step of
tumor glycolysis, was significantly decreased in GC cells following treatment with β-
asarone. Mechanistically, β-
asarone can reduce
pyruvate dehydrogenase kinase (PDK) 1, phospho(p)-PDK1, PDK4,
hypoxia-inducible factor 1-α (HIF1α), c-myc, STAT5, and p-STAT5 expression, which revealed how β-
asarone affects
tumor glycolysis. In conclusion, the present study provided evidence in support of the hypothesis that the increase of
chemotherapy sensitization by β-
asarone is associated with the inhibition of
tumor glycolysis.