Emodin regulates cell cycle of non-small lung cancer (NSCLC) cells through hyaluronan synthase 2 (HA2)-HA-CD44/receptor for hyaluronic acid-mediated motility (RHAMM) interaction-dependent signaling pathway

摘要

Effect of emodin on the cell viability and HA secretion of lung cancer cells. Lung cancer cell lines were exposed to 0–30 µM emodin for 24 h before the MTT and ELISA assay. a Suppression of emodin on cell viability of lung cancer cell lines. A549 was the most sensitive cell line with an effective concentration of 5 µM. Viability of A549 was dose-dependently inhibited by emodin at 5–30 mM. H520 was the second most sensitive cell line with an effective concentration of 15 µM. Viability of H520 was dose-dependently inhibited by emodin at 15–30 mM. The other three cell lines, including H1975, H1299, and H460, showed a significant decrease in cell viability only when the concentration of emodin reached 30 µM. b The effect of emodin on apoptosis. Emodin at 20–30 mM had a slight apoptosis induction effect (< 20%) on all cell lines. The apoptosis induction of emodin was not different among cell lines. c The effect of emodin on HA secretion of lung cancer cells. Emodin at 30 µM suppressed HA secretion in all lung cancer cell lines tested except for H460, inferring that emodin might regulate HA generation. A549 was the most sensitive cell line with a suppression rate of over 75%. “*” marks the significant difference (p < 0.05) compare with the control (0 µM or “−”)