The oncogenic role of the long noncoding RNA associated with poor prognosis of hepatocellular carcinoma (lncRNA AWPPH) was reported in various types of malignancies; however, its involvement in ovarian carcinoma (OC) remains unknown. Thus, the present study investigated the role of AWPPH in OC. The expression of AWPPH in tissues and serum acquired from patients with OC, and healthy controls, was determined via reverse transcription-quantitative polymerase chain reaction. The diagnostic value of serum AWPPH expression was evaluated by receiver operating characteristic curve analysis. Additionally, survival curve analysis was performed to determine the prognostic value of AWPPH for OC. An AWPPH overexpression vector was transfected into OC cell lines. Cell proliferation, migration and invasion were analyzed via Cell Counting Kit-8, Transwell migration and invasion assays, respectively. The expression of β-catenin was investigated via western blotting. It was revealed that the expression levels of AWPPH were significantly upregulated in OC tissues and serum compared with healthy controls. The serum levels of AWPPH were able to effectively diagnose and predict the prognosis of patients with OC. AWPPH overexpression promoted the proliferation, migration and invasion of OC cells, and upregulated β-catenin expression. Treatment with a Wnt agonist markedly altered AWPPH expression; however, inhibition of Wnt suppressed the effects of AWPPH overexpression on proliferation, migration and invasion of OC cells. Therefore, it was revealed that AWPPH may promote OC via activation of the Wnt/β-catenin signaling pathway.

Epithelial-mesenchymal transition (EMT) has been shown to exert promoting effects on the progression of a number of cancer types, including endometrial carcinoma (EC). MicroRNA (miRNA or miR)-195 has been shown to function as a tumor suppressor. This study aimed to explore the potential role of miR-195 in the EMT process of EC. miR-195 overexpression (Mimics) and mimics control (Mock) vectors were constructed and transfected into human endometrial cancer cells (AN3-CA and Hec1A) using Lipofectamine 2000, and cell viability was detected using the Cell Counting kit-8 (CCK-8). The invasive and migratory capacities of the cells transfected with the Mimics or Mock vectors were assessed by Transwell and wound healing assays. Relative mRNA and protein levels were analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, respectively. Using TargetScan prediction, the potential target of miR-195 was identified and was further verified by dual-luciferase reporter assay. Following transfection with miR-195 mimics, the viability of the AN3-CA and Hec1A cells decreased in a time-dependent manner, specifically at 24 h. The wound closure rate and the number of invaded cells in the Mimics group were much lower than those in the Control and Mock groups (P<0.01). miR-195 overexpression significantly upregulated the mRNA and protein levels of tissue inhibitor of metalloproteinase 2 (TIMP-2), while it downregulated the expression levels of matrix metalloproteinase (MMP)-2 and MMP-9. Moreover, the phosphorylation levels of PI3K and AKT were also notably decreased (P<0.01). G protein-coupled estrogen receptor 1 (GPER) was identified as a target of miR-195. On the whole, the findings of this study indicate that the inhibitory effects of miR195 on EC cell migration and invasion are associated with the PI3K/AKT signaling pathway and GPER expression.