[No authors listed]
Endometrial cancer (EC) is a common form of cancer in women. Metastasis is the main cause of EC treatment failure. Eukaryotic translation initiation factor 4E (eIF4E) is an oncogene that is overexpressed in a variety of malignancies and their distant metastases. The present study analyzed microarray data from the Oncomine database and revealed that high eIF4E expression was associated with poor prognosis and high pathological grade of EC. The expression of eIF4E was higher in EC tissues compared with in adjacent normal tissues. In addition, microRNA (miR)â320a and miRâ340â5p expression levels were downregulated in EC tissues compared with those in adjacent normal tissues, which suggested that these microRNAs may serve as EC tumor suppressor genes. miRâ320a and miRâ340â5p could bind to the 3'âUTR of eIF4E mRNA, thus downregulating the expression of eIF4E and phosphorylated (p)âeIF4E in EC cells. Overexpression of miRâ320a or miRâ340â5p effectively suppressed HECâ1A cell migration and invasion. The downregulation of eIF4E and pâeIF4E following miRâ320a or miRâ340â5p transfection reduced the invasiveness and metastatic capability of EC cells in a manner associated with decreased expression of matrix metallopeptidase (MMP)â3 and MMPâ9. In addition, one of the effects of transforming growth factor β1 (TGFâβ1), which is to induce the phosphorylation of eIF4E, was suppressed by miRâ320a and miRâ340â5p overexpression. These two microRNAs also attenuated the features of TGFâβ1âinduced epithelialâmesenchymal transition (EMT). In conclusion, the results of the present study demonstrated that eIF4E was upregulated in EC, whereas miRâ320a and miRâ340â5p were downregulated in EC compared with adjacent normal tissues. In vitro, miRâ320a and miRâ340â5p inhibited the migratory capability of EC cells by downregulating MMPâ3 and MMPâ9 and prevented TGFâβ1âinduced EMT through pâeIF4E.
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