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MicroRNA‐183 induces epithelial‐mesenchymal transition and promotes endometrial cancer cell migration and invasion in by targeting CPEB1

The aim of this study is to evaluate the ability of microRNA‐183 (miR‐183) to influence epithelial‐mesenchymal transition (EMT) and cell proliferation, migration, invasion, and apoptosis in endometrial cancer (EC) by targeting cytoplasmic polyadenylation element binding protein 1(CPEB1). EC tissues with matched nonmalignant tissues were collected from 208 EC patients. Ishikawa and RL95‐2 cells were selected for cell experiments in vitro and each kind of cells were grouped into blank, negative control (NC), miR‐183 mimic, miR‐183 inhibitor, CPEB1 overexpression, and miR‐183 mimic + CPEB1 overexpression groups. Expressions of miR‐183, CPEB1, E‐cadherin, and Vimentin were determined by reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and Western blotting. Cell viability, colony formation ability, migration, invasion, and apoptosis were assessed by MTT assay, clone formation assay, scratch test, Transwell assay, and flow cytometry. In vivo tumorigenesis of Ishikawa cells was evaluated by tumor formation in nude mice. The miR‐183 expression was higher, but the CPEB1 expression was lower in EC tissues than in adjacent nonmalignant tissues. CPEB1 was confirmed as the target of miR‐183 by dual‐luciferase reporter assay. The miR‐183 mimic group had increased cell viability, colony formation ability, cell invasion and migration, tumor volume and weight in nude mice, but decreased cell apoptosis when compared with the blank group. The expression of E‐cadherin was down‐regulate, but expression of Vimentin was up‐regulate in the miR‐183 mimic group in comparison with the blank group. In terms of a comparison between the blank group and CPEB1 overexpression group, the CPEB1 overexpression group had suppressed cell viability, colony formation ability, cell invasion and migration, tumor volume and weight, but increased cell apoptosis. The expression of E‐cadherin was up‐regulated, but the expression of Vimentin was down‐regulated in the CPEB1 overexpression group in comparison with the blank group. The miR‐183 mimic + CPEB1 overexpression group had higher miR‐183 expression than the blank group. These findings indicate that miR‐183 induces EMT, inhibits apoptosis, and promotes cell proliferation, migration, invasion, and in vivo tumorigenesis in EC by targeting CPEB1.