Endometrial cancer (EC) is one of the three most common gynecological cancers. Due to the lack of effective treatment for EC patients in an advanced stage, the mortality rate of EC is increasing rapidly. Hence, it is essential to seek for novel molecular therapeutic targets and biomarkers for EC. The aim of this study was to explore the role of miR-218 in the occurrence and development of EC and to investigate the possible underlying mechanism.,The expression level of miR-218 in EC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Wound healing assay and Matrigel assay were performed to determine the migration and invasion abilities of EC cells. Meanwhile, the po... More
Endometrial cancer (EC) is one of the three most common gynecological cancers. Due to the lack of effective treatment for EC patients in an advanced stage, the mortality rate of EC is increasing rapidly. Hence, it is essential to seek for novel molecular therapeutic targets and biomarkers for EC. The aim of this study was to explore the role of miR-218 in the occurrence and development of EC and to investigate the possible underlying mechanism.,The expression level of miR-218 in EC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Wound healing assay and Matrigel assay were performed to determine the migration and invasion abilities of EC cells. Meanwhile, the potential targets of miR-218 were predicted by bioinformatics analysis and confirmed by Luciferase reporter gene assay. In addition, the protein expression level of Adducin 2 (ADD2) was assessed by Western blotting analysis.,QRT-PCR results revealed that miR-218 was significantly downregulated in EC tissues and cell lines. Wound healing assay and Matrigel assay demonstrated that miR-218 suppressed the migration and invasion abilities of EC cells. Online prediction databases predicted that ADD2 was a direct target of miR-218, which was verified by Luciferase reporter gene assay. Rescue experiments further validated that miR-218 could serve as a carcinoma suppressor by negatively regulating ADD2 expression in EC.,In the present study, we elucidated that miR-218 served as a tumor suppressor in EC by negatively regulating ADD2. This might bring a novel insight into new molecular therapeutic targets and biomarkers for EC.
