OBJECTIVE: Recently, long noncoding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA OR3A4 in the development of ovarian cancer (OC), and to explore the possible underlying mechanism. PATIENTS AND METHODS: OR3A4 expression in OC tissue samples was detected by Real-time quantitative polymerase chain reaction (qRT-PCR). Moreover, wound healing assay and transwell assay were performed to evaluate the effect of OR3A4 on the metastasis of OC. Furthermore, the underlying mechanism was explored by RT-qPCR and Western blot assay. RESULTS: The expression level of OR3A4 in OC samples was significantly higher than that of adjacent tissues. Moreover, cell migration and invasion were significantly repressed after OR3A4 knockdown in vitro. Moreover, the mRNA and protein expressions of kruppel-like factor 6 (KLF6) were remarkably upregulated after knockdown of OR3A4. Furthermore, the expression level of KLF6 was negatively correlated with the expression of OR3A4 in OC tissues. CONCLUSIONS: Our results showed that OR3A4 could enhance OC cell metastasis and invasion via suppressing KLF6. Moreover, OR3A4 might be a potential therapeutic target for OC.
OBJECTIVE: Recently, long noncoding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA OR3A4 in the development of ovarian cancer (OC), and to explore the possible underlying mechanism. PATIENTS AND METHODS: OR3A4 expression in OC tissue samples was detected by Real-time quantitative polymerase chain reaction (qRT-PCR). Moreover, wound healing assay and transwell assay were performed to evaluate the effect of OR3A4 on the metastasis of OC. Furthermore, the underlying mechanism was explored by RT-qPCR and Western blot assay. RESULTS: The expression level of OR3A4 in OC samples was significantly higher than that of adjacent tissues. Moreover, cell migration and invasion were significantly repressed after OR3A4 knockdown in vitro. Moreover, the mRNA and protein expressions of kruppel-like factor 6 (KLF6) were remarkably upregulated after knockdown of OR3A4. Furthermore, the expression level of KLF6 was negatively correlated with the expression of OR3A4 in OC tissues. CONCLUSIONS: Our results showed that OR3A4 could enhance OC cell metastasis and invasion via suppressing KLF6. Moreover, OR3A4 might be a potential therapeutic target for OC.