Effect of Momordica charantia protein on proliferation, apoptosis and the AKT signal transduction pathway in the human endometrial carcinoma ishikawa H cell line in vitro

Abstract

Endometrial carcinoma (EC) is one of the most common female malignancies, and there is an urgent requirement to explore new therapeutic strategies. In the present study, Ishikawa H cells were treated with Momordica charantia protein (MCP30). The cell morphology, growth inhibition rate, cell cycle distribution, and expression of phosphate and tensin homolog, P-AKT and AKT were measured. DNA fragmentation analysis and Annexin V-fluorescein isothiocyanate/propidium iodide double staining assay were used to analyze cell apoptosis. MCP30 decreased the viability of Ishikawa H cells in a dose- and time-dependent manner. The early apoptotic rates of Ishikawa H cells treated with MCP30 at 666.67 pM reached to 16.07±0.15%, following 72 h of treatment. DNA ladder was observed in cells treated with 333.33 and 666.67 pM MCP30 following 72 h of treatment. MCP30 blocks Ishikawa H cells from progressing between the S-phase and the G2/M-phase in a time- and concentration-dependent manner. Western blotting revealed that MCP30 treatment decreased the levels of P-AKT in a dose-dependent manner. It was revealed that MCP30 decreases cell proliferation, and induces apoptosis and S-phase cell cycle arrest through the AKT signaling pathway in Ishikawa H cells.