LncRNA MIF-AS1 aggravates the progression of ovarian cancer by sponging miRNA-31-5p.

OBJECTIVE:The aim of this study was to uncover the role of lncRNA MIF-AS1 in influencing the biological phenotypes of ovarian cancer (OC) and the underlying mechanism. PATIENTS AND METHODS:OC tissues and adjacent normal tissues were collected from 50 OC patients. The expression level of lncRNA MIF-AS1 in OC tissues and cells was determined by quantitative Real-Time (qRT-PCR). The prognostic potential of MIF-AS1 in OC patients was assessed by the Kaplan-Meier method. Subsequently, the regulatory effects of MIF-AS1 on proliferative, migratory, and invasive abilities of ES-2 and HO-8910 cells were evaluated by a series of functional experiments. Dual-Luciferase reporter gene assay, qRT-PCR, and Western blot were further conducted to verify the interaction in the regulatory loop MIF-AS1/miRNA-31-5p/PLCB1. RESULTS:MIF-AS1 was significantly upregulated in OC tissues and cell lines (p<0.05). Higher level of MIF-AS1 predicted significantly worse prognosis of OC patients (p<0.05). The knockdown of MIF-AS1 markedly attenuated the proliferative, migratory, and invasive abilities of ES-2 and HO-8910 cells (p<0.05). Dual-Luciferase reporter gene assay verified that MIF-AS1 competed with PLCB1 to bind miRNA-31-5p. In addition, MIF-AS1 negatively regulated miRNA-31-5p expression cells, and miRNA-31-5p negatively regulated PLCB1 expression in OC. CONCLUSIONS:MIF-AS1 was significantly upregulated in OC, which accelerated the proliferative, migratory, and invasive abilities of OC cells. Furthermore, the regulatory loop MIF-AS1/miRNA-31-5p/PLCB1 could be utilized as a therapeutic target for OC.

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