extracts induce cell cycle arrest and apoptosis in human esophageal squamous carcinoma ECA-109 cells via the PI3K/AKT/mTOR signaling pathway.

Recently, ethyl acetate extracts (COE) have been investigated for their anticancer effects on digestive tract tumors. However, the therapeutic effects of COE on esophageal squamous carcinoma cells (ESCC) have not been investigated. In the present study, the effects of COE on the cell cycle and apoptosis of ESCCs were assessed , and it was revealed that COE treatment triggered G/G cell cycle arrest, and induced DNA damage and apoptosis in a dose-dependent manner in ESCC. Activation of the phosphatidylinositol 3-kinase/protein kinase-B/mechanistic target of rapamycin (mTOR) pathway was also suppressed by COE. Additionally, the combined treatment with COE and rapamycin (an mTOR inhibitor) acted synergistically in ECA-109 cells compared with the treatment with COE or rapamycin alone. These findings extend the understanding of the action of COE and suggest that COE has potential as a treatment option for ESCC as a single treatment or in combination.