| Summary: | Background: In recent years, a large number of studies have shown that differentially expressed lncRNAs in tumors are capable of inducing tumorigenesis and promoting tumor development. However, the role of LINC01210 in OC still remains unclear. Methods: Relative levels of LINC01210 and KLF4 in OC tissues containing in the GSE40595 dataset and those collected in our hospital were determined. Prognostic potential of LINC01210 in OC was evaluated by Kaplan-Meier method. Correlation between expression levels of LINC01210 and KLF4 was assessed by Spearman correlation test. After silence of LINC01210 in A2780 and HO8910 cells, changes in proliferative, migratory and invasive abilities were examined. Moreover, the interaction between LINC01210 and KLF4 was explored by RIP and ChIP. Rescue experiments were conducted to uncover the involvement of KLF4 in LINC01210-regulated OC progression. Results: LINC01210 was upregulated in OC tissues and KLF4 was downregulated. LINC01210 level was higher in OC patients with metastases or advanced stage. Besides, its level was negatively correlated to DFS (disease-free survival) and OS (overall survival) of OC patients. Silence of LINC01210 attenuated proliferative, migratory and invasive abilities in A2780 and HO8910 cells. Through analyzing the GSE40595 dataset, LINC01210 was found to be negatively linked to KLF4. RIP assay further verified the interaction between LINC01210 and KLF4. Knockdown of LINC01210 markedly decreased the recruitment ability of EZH2 to KLF4. Importantly, silence of KLF4 could reverse regulatory effects of LINC01210 on cellular behaviors of OC. Conclusions: LINC01210 is upregulated in OC and predicts a poor prognosis. It accelerates proliferation, invasion and migration in OC cells through epigenetically downregulating KLF4.
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