The Effect of FERMT1 Regulated by miR-24 on the Growth and Radiation Resistance of Esophageal Cancer

The present study addresses the role and underlying mechanism of FERMT1 in the development of esophageal cancer (EC). High level of FERMT1 expression was found in human EC tissues and was significantly correlated with poor overall survival. Overexpression of FERMT1 by a lentiviral vector markedly promoted EC cell proliferation and radiation resistance in vitro and facilitated tumor growth in vivo. Using the luciferase assay, we further documented that microRNA-24 (miR-24) suppressed the expression of FERMT1 through direct binding to the 3 -untranslated region (3 -UTR) of its mRNA. While forced miR-24 expression suppressed cell growth and enhanced the radiosensitivity of EC cells, re-expression of FERMT1 reversed these effects. Together, our data indicate that FERMT1 acts as an oncogene and is negatively regulated by miR-24, supporting the potential therapeutic strategy against esophageal cancer by targeting miR-24-FERMT1 axis.