Inhibition of mammalian target of rapamycin by rapamycin increases the radiosensitivity of esophageal carcinoma Eca109 cells

The aim of the present study was to investigate whether radiation induces the mammalian target of rapamycin (Rap) (mTOR) signaling pathway in esophageal carcinoma Eca109 cells, and whether mTOR inhibition by rapamycin increases Eca109 cell radiosensitivity. Changes in the levels of mTOR signaling pathway and DNA damage-repair proteins in Eca109 cells prior to and following radiation were determined. The Eca109 cells were treated with Rap (0, 100, 200 and 400 nmol/l) in combination with radiation (0, 2, 4 and 6 Gy). The cell proliferation inhibition rate was determined by MTT assay. The optimum Rap concentration and radiation dose, which appropriately inhibited cell proliferation, were then selected for further study. An appropriate combination of Rap and radiation for the Eca109 cells was also selected and changes in the mTOR signaling pathway, apoptosis and DNA damage-repair proteins, as well as in cell clone formation, survival curves, the apoptosis rate and radiation-induced DNA damage were determined. The expression of the mTOR signaling pathway and DNA damage-repair proteins were found to increase following the irradiation of the Eca109 cells. In addition, Rap was found to inhibit the mTOR signaling pathway and the expression of the DNA damage-repair proteins. At the same radiation dose, with increasing Rap concentration, the proliferation inhibition rates of the Eca109 cells were found to improve. The clone formation and survival curves of the experimental group were less than those of the control groups. Furthermore, the cell apoptosis rate and expression of cleaved caspase-3 and bax in the experimental group were higher than those of the control groups, whereas the expression of bcl-2 was less than that of the control groups. The radiation-induced DNA damage of the experimental group was greater than that of the control group. The inhibition of mTOR by Rap was found to effectively inhibit the proliferation, survival and radiation-induced DNA damage repair of the Eca109 cells following irradiation, as well as promoting radiation-induced apoptosis, thereby increasing the radiosensitivity of the esophageal carcinoma Eca109 cells.