Inhibitory Effect and Mechanism of Forsythin on Malignantly Transformed Esophageal Epithelial Cells and Esophageal Cancer Eca-109 Cells

The inhibitory effect of forsythin on the proliferation, cell cycle, apoptosis, migration and invasion of malignantly transformed esophageal epithelial cells and esophageal cancer Eca-109 cells was explored, and the underlying mechanism was analyzed.

Malignantly transformed esophageal epithelial cells and Eca-109 cells were treated with 10 and 100 μmol/L forsythin for 24 h. Cell proliferation was detected by cell counting kit-8 (CCK-8). Cell cycle and apoptosis were detected by flow cytometry. Cell migration and invasion were detected by Transwell method. The expression levels of phosphoinositide 3-kinase (PI3K), protein kinase B (PKB, also known as AKT), phosphorylated phosphatidylinositol-3-kinase (p-PI3K), phosphorylated protein kinase B (p-PKB, also knoun as p-AKT), p21, B-cell lymphoma-2 (Bcl-2), and matrix metallopeptidase 9 (MMP9) in cells were detected by Western blotting.

The 50% inhibitory concentration (IC₅₀) values of forsythin for malignantly transformed esophageal epithelial cells and Eca-109 cells were 308.4 and 322.0 μmol/L, respectively. Forsythin at 10 and 100 μmol/L could significantly inhibit the proliferation of the two cell lines (P < 0.05), but was nontoxic to normal esophageal epithelial cells. Forsythin at 10 and 100 μmol/L could alter cell cycle, promote cell apoptosis, significantly inhibit cell migration and invasion (P < 0.05), and reduce the expression levels of p-PI3K, p-AKT, Bcl-2 and MMP9 proteins (P < 0.05). Forsythin at 100 μmol/L could significantly increase the expression level of p21 protein in both cell lines (P < 0.05).

Forsythin can significantly inhibit the proliferation, migration and invasion of esophageal epithelial malignant transformed cells and Eca-109 cells, and the mechanism may be related to the inactivation of the PI3K/AKT pathway.