Researchers have determined the promising therapeutic potential of targeting c-Met in radiochemotherapy resistant esophageal cancer patients.
Esophageal cancer is the eighth most common malignancy and the sixth most common cause of death worldwide. While surgery represents the primary modality of treatment, the prognosis and survival for this disease remains poor. Radiotherapy has been a critical treatment option for those unresectable esophageal cancer patients. c-Met, a receptor tyrosine kinase (RTK) encoded by MET gene, mediates cell proliferation, survival, invasion and has been considered to play a role in the metastasis and relapse of esophageal cancer.
A study led by Dr. Xin-Chen Sun and published in the Journal of Cancer 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. In vivo studies confirmed that the combinatorial use of foretinib with irradiation significantly diminishes tumour burden compared to either treatment alone.
The findings from this study imply a crucial role of c-Met in the modulation of radiosensitization in esophageal cancer, and foretinib as a potential radiosensitizer for the treatment of esophageal cancer.