Baicalein suppresses rectal cancer progression through inhibition of cellular glycolysis and intracellular adenosine triphosphate level

Abstract

This study explored the mechanism of baicalein on rectal cancer. Human rectal adenocarcinoma cells HR8348 were exposed to low, moderate and high concentration of baicalein (5, 10, and 20 μmol/L), respectively, for 48 h with untreated control group, followed by analysis of glucose consumption, lactic acid and denosine triphosphate (ATP) content, cell proliferation and expression of phosphatidylinositol-3-kinase (PI3K), protein kinase B(AKT), and Hypoxia-Inducible Factor 1-Alpha (HIF-1α). Cell viability in groups of baicalein decreased at 24, 48, and 72 h after treatment, with lowest cell viability in high-dose group (P <0.05), especially at 48 and 72 h in both medium and high dose groups (P <0.05). Of note, baicalein dose-dependently induced cell apoptosis and reduced levels of PI3K, AKT, and HIF-1α. Moreover, glucose consumption and lactic acid content gradually decreased in the absence of baicalein, and the increased concentration of baicalein was associated with more dramatical decrease in glucose consumption. The lowest glucose consumption [(6.49±2.23) μmol/105 cells] and lactic acid content [(16.90±3.77) μmol/105 cells] was noticed in the high-dose group. Baicalein decreased ATP content, facilitating energy metabolism in rectal cancer cells (P <0.05). Baicalein inhibits PI3K/Akt pathway to down-regulate HIF-1α, thereby suppressing cell viability and proliferation of rectal cancer HR8348 cells. This is due to inhibition of glycolysis and intracellular energy metabolism, which provides a new insight into new treatment method for rectal cancer.