Oncology Reports · 2018 · 42 citations · 30 references
MedicineCancer BiologyOncologyGene ExpressionMetastasisMolecular OncologyCancer GenomicsCancer TranscriptomicsMalignant NeoplasmsNoncoding Rna In CancerOvarian CancerOvarian NeoplasiaCancer-related Noncoding Rna FunctionLuciferase Reporter AssaysLung AdenocarcinomaMalignant Ovarian NeoplasmsMalignant Ovarian TumorsMicrorna Function In CancerMicrorna In CancerNoncoding Rna Expression Profiling
Epithelial ovarian cancer (EOC) is one of the most lethal malignancies of the female reproductive organs. Increasing evidence has revealed that long non‑coding RNAs (lncRNAs) participate in tumorigenesis. Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is an lncRNA and plays a role in various types of tumors. However, the function of MALAT1 on cellular behavior in EOC remains unclear. The current study explored the expression of MALAT1 in ovarian cancer tissues and in EOC cell lines. Quantitative RT‑PCR analysis revealed that the expression of MALAT1 was higher in human ovarian malignant tumor tissues and EOC cells than in normal ovarian tissues and non‑tumorous human ovarian surface epithelial cells, respectively. By analyzing the online database Kaplan‑Meier Plotter, MALAT1 was identified to be correlated with the overall survival (OS) and progression‑free survival (PFS) of patients with ovarian cancer. Furthermore, knockdown of MALAT1 by small interfering RNA (siRNA) significantly decreased EOC cell viability, migration, and invasion. Finally, dual‑luciferase reporter assays demonstrated that MALAT1 interacted with miR‑143‑3p, a miRNA that plays a role in EOC as demonstrated in our previous study. Inhibition of MALAT1 resulted in an increase of miR‑143‑3p expression, leading to a decrease of CMPK protein expression. In conclusion, our results indicated that MALAT1 was overexpressed in EOC. Silencing of MALAT1 decreased EOC cell viability and inhibited EOC cell migration and invasion. These data revealed that MALAT1 may serve as a new therapeutic target of human EOC.
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