Exosomal-miR-32-5p directly targets FOXN2 to regulate the proliferation, migration and apoptosis of uterine corpus endometrial carcinoma via the PI3K/AKT/BCL-2 pathway

外泌体 miR-32-5p 通过 PI3K/AKT/BCL-2 通路直接靶向 FOXN2,调控子宫内膜癌细胞的增殖、迁移和凋亡。

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Abstract

The transfer of microRNAs (miRNAs) between cells through exosomes is crucial in controlling the expression of various target genes in the recipient cells, giving exosomal miRNAs the capability to control the advancement of tumors. The present study aimed to explore the function of exosomal miR-32-5p in the in vitro progression of uterine corpus endometrial carcinoma (UCEC). Bioinformatics analyses were applied to identify potential miRNAs in UCEC. Forkhead Box N2 (FOXN2) was subsequently predicted as a putative target gene of miR-32-5p, followed by examination through a luciferase reporter assay. Exosomes derived from UCEC cells or plasma samples of patients with UCEC were examined. The biological functions of miR-32-5p or exosomal miR-32-5p were determined by cell phenotype experiments. Protein and mRNA expression in UCEC cells were assessed through western blotting and quantitative reverse transcription-PCR, respectively. miR-32-5p demonstrated the most significant effects on survival probability, therefore it was selected for further investigation in in the present study. miR-32-5p was observed to be enriched in plasma exosomes and significantly upregulated in cancer tissues, as well as in cancer plasma exosomes. The present findings demonstrated that exosomal-miR-32-5p could induce the proliferation, migration and suppress apoptosis of UCEC cells through regulation of the FOXN2/PI3K/AKT/Bcl-2 pathway, thus exhibiting potential as therapeutic target against UCEC.

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