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https://www.selleckchem.com/products/cc-115.html Up-regulated miR-202-5p inhibited cell proliferation and metastasis in vitro. HOXB2 was a downstream target of miR-202-5p. CONCLUSIONS We verified that miR-202-5p suppressed cell proliferation, migration, and invasion in OC via regulating HOXB2. Our findings provide new insights into the underlying mechanism of OC progression and may be useful in finding biomarkers and therapeutic targets of OC.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 Polymerase Chain Reaction (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 less then 0.05). Higher level of MIF-AS1 predicted significantly worse prognosis of OC patients (p less then 0.05). The knockdown of MIF-AS1 markedly attenuated the proliferative, migratory, and invasive abilities of ES-2 and HO-8910 cells (p less then 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. Fur

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