Y Tian1, Y-R Wang, S-H Jia. 1. Department of Histology and Embryology, Changzhi Medical College, Changzhi, China. 905066445@qq.com.
Abstract
OBJECTIVE: Recently, the vital role of long noncoding RNAs (lncRNAs) in human diseases have got much attention. In this research, lncRNA DLX6-AS1 is studied to verify how it affects the development of cervical cancer (CC). PATIENTS AND METHODS: DLX6-AS1 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in both CC cells and tissue samples. Besides, functional experiments including cell counting kit-8 (CCK-8) assay, colony formation assay, and transwell assay were performed. Meanwhile, the underlying mechanism was explored through qRT-PCR and Western blot assay. The function of DLX6-AS1 was also identified in vivo. RESULTS: By comparing with corresponding tissues, the DLX6-AS1 expression level was significantly higher in CC samples. Moreover, cell growth ability and invaded ability of CC cells were inhibited after DLX6-AS1 was knocked down. Furthermore, the expression of FUS was inhibited after knockdown of DLX6-AS1. It was found that the expression level of FUS positively correlated to the expression of DLX6-AS1 in CC tissues. In addition, knockdown of DLX6-AS1 inhibited tumor formation and metastasis of CC in nude mice. CONCLUSIONS: These results suggest that DLX6-AS1 could enhance cell proliferation and metastasis of CC by upregulating FUS, which might be a potential therapeutic target in CC.
OBJECTIVE: Recently, the vital role of long noncoding RNAs (lncRNAs) in human diseases have got much attention. In this research, lncRNA DLX6-AS1 is studied to verify how it affects the development of cervical cancer (CC). PATIENTS AND METHODS: DLX6-AS1 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in both CC cells and tissue samples. Besides, functional experiments including cell counting kit-8 (CCK-8) assay, colony formation assay, and transwell assay were performed. Meanwhile, the underlying mechanism was explored through qRT-PCR and Western blot assay. The function of DLX6-AS1 was also identified in vivo. RESULTS: By comparing with corresponding tissues, the DLX6-AS1 expression level was significantly higher in CC samples. Moreover, cell growth ability and invaded ability of CC cells were inhibited after DLX6-AS1 was knocked down. Furthermore, the expression of FUS was inhibited after knockdown of DLX6-AS1. It was found that the expression level of FUS positively correlated to the expression of DLX6-AS1 in CC tissues. In addition, knockdown of DLX6-AS1 inhibited tumor formation and metastasis of CC in nude mice. CONCLUSIONS: These results suggest that DLX6-AS1 could enhance cell proliferation and metastasis of CC by upregulating FUS, which might be a potential therapeutic target in CC.