As a crucial event involved in the
metastasis and relapse of
esophageal cancer, c-Met overexpression has been considered as one of the culprits responsible for the failure in patients who received
radiochemotherapy. Since c-Met has been confirmed to be pivotal for cell survival, proliferation and migration, little is known about its impact on the regulation of radiosensitivity in
esophageal cancer. The present study investigated the radiosensitization effects of c-Met inhibitor
foretinib in ECA-109 and TE-13 cell lines.
Foretinib inhibited c-Met signaling in a dose-dependent manner resulting in decreases in the cell viability of ECA-109 and TE-13. Pretreatment with
foretinib synergistically prompted cell apoptosis and G2/M arrest induced by irradiation. Moreover, decreases ability of DNA damage repair was also observed. In vivo studies confirmed that the combinatorial use of
foretinib with irradiation significantly diminishes
tumor burden compared to either treatment alone. The present findings implied a crucial role of c-Met in the modulation of radiosensitization in
esophageal cancer, and
foretinib increased the radiosensitivity in ECA-109 and TE-13 cells mainly via c-Met signaling, highlighting a novel profile of
foretinib as a potential radiosensitizer for the treatment of
esophageal cancer.