RESUMO
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)320a and miR3405p 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. miR320a and miR3405p could bind to the 3'UTR of eIF4E mRNA, thus downregulating the expression of eIF4E and phosphorylated (p)eIF4E in EC cells. Overexpression of miR320a or miR3405p effectively suppressed HEC1A cell migration and invasion. The downregulation of eIF4E and peIF4E following miR320a or miR3405p transfection reduced the invasiveness and metastatic capability of EC cells in a manner associated with decreased expression of matrix metallopeptidase (MMP)3 and MMP9. In addition, one of the effects of transforming growth factor ß1 (TGFß1), which is to induce the phosphorylation of eIF4E, was suppressed by miR320a and miR3405p overexpression. These two microRNAs also attenuated the features of TGFß1induced epithelialmesenchymal transition (EMT). In conclusion, the results of the present study demonstrated that eIF4E was upregulated in EC, whereas miR320a and miR3405p were downregulated in EC compared with adjacent normal tissues. In vitro, miR320a and miR3405p inhibited the migratory capability of EC cells by downregulating MMP3 and MMP9 and prevented TGFß1induced EMT through peIF4E.