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However, the role of <jats:italic>EIF1AX<\/jats:italic> in endometrial carcinoma (EC) remains unknown. We investigated the <jats:italic>EIF1AX<\/jats:italic> expression in EC patients and assessed its tumorigenesis\u2010associated function and nucleocytoplasmic transport mechanism <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic>. The results indicated that the cytoplasmic EIF1AX expression showed a gradual increase when going from endometrium normal tissue, simple endometrial hyperplasia, complex endometrial hyperplasia, and endometrial atypical hyperplasia to EC, while vice versa for the nuclear EIF1AX expression. In addition, the cytoplasmic EIF1AX expression was positively correlated with histologic type, high International Federation of Gynecology and Obstetrics (FIGO) grade, advanced FIGO stage, deeper infiltration, high Ki67 index, and shorter recurrence\u2010free survival in EC patients. <jats:italic>In vitro<\/jats:italic>, short hairpin RNA\u2010mediated <jats:italic>EIF1AX<\/jats:italic> depletion or SV40NLS\u2010mediated EIF1AX import into the nucleus in multiple human EC cells potently suppressed cell migration and invasion, epithelial\u2010mesenchymal transition, and lung metastasis. Moreover, exportin 1 induced the transport of EIF1AX from the nucleus to the cytoplasm that could be inhibited by leptomycin B treatment or the mutation in the <jats:italic>EIF1AX<\/jats:italic> location sequence. These results demonstrate that cytoplasmic EIF1AX may play a key role in the incidence and promotion of EC, and thus, targeting EIF1AX or its nucleocytoplasmic transport process may offer an effective new therapeutic approach to EC.<\/jats:p>","DOI":"10.1155\/2022\/1361135","type":"journal-article","created":{"date-parts":[[2022,12,22]],"date-time":"2022-12-22T13:50:09Z","timestamp":1671717009000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["XPO1\u2010Mediated EIF1AX Cytoplasmic Relocation Promotes Tumor Migration and Invasion in Endometrial 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