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Objective:To investigate the clinical significance and biological effect of long non-coding RNA (lncRNA) NRSN2-AS1 in ovarian cancer.Methods:The expression of NRSN2-AS1 was detected by real-time quantitative PCR (RT-qPCR) in 84 cases of ovarian cancer tissues and corresponding normal adjacent tissues, and the relationship between NRSN2-AS1 expression and clinical data of patients was analyzed. Human ovarian epithelial cells HOSEpiC and human ovarian cancer cells A2780 and OVCAR3 were cultured in vitro, and overexpression or interference of NRSN2-AS1 and control plasmids were respectively transfected into A2780 and OVCAR3 cells as the blank group, overexpression group and control group, interference group. CCK-8 assay was used to detect cell proliferation, while transwell invasion and migration assay were used to detect the change of cell metastasis ability, RT-qPCR and Western blot were used to detect the expressions of SRY related HMG box transcription factor 12 (SOX12), a potential downstream gene of NRSN2-AS1.Results:The expressions of NRSN2-AS1 in ovarian cancer tissues and cells were significantly higher than normal adjacent tissues, and the high expression of NRSN2-AS1 was significantly correlated with poor prognosis, lymph node metastasis and high clinical stage ( P<0.05). In the blank and overexpression group, the expressions of NRSN2-AS1 were 1.00±0.08 and 5.78±0.41, the expressions of SOX12 mRNA were 1.00±0.10 and 3.08±0.23, the expression of SOX12 protein were 1.00±0.08 and 7.26±0.39, the invasion cells per field were 22.7±4.9 and 79.0±6.2, and the migration cells per field were 26.5±4.1 and 43.5±4.5. In the control and interference group, the expression of NRSN2-AS1 were 1.00±0.11 and 0.37±0.04, the expressions of SOX12 mRNA were 1.00±0.07 and 0.59±0.05, the expression of SOX12 protein were 1.00±0.07 and 0.36±0.03, the invasion cells per field were 68.3±6.1 and 30.6±5.5, and the migration cells per field were 85.2±7.0 and 22.7±4.2. Compared with the blank group, the expression of SOX12 mRNA and protein in the overexpression group was significantly increased ( P<0.05), and the cell proliferation and metastasis ability were significantly enhanced ( P<0.05). Compared with the control group, the expression of SOX12 mRNA and protein in the interference group was significantly decreased, and the ability of cell proliferation and metastasis was suppressed significantly ( P<0.05) . Conclusion:The expression of NRSN2-AS1 is up-regulated in ovarian cancer, which is closely related to poor prognosis and progression of ovarian cancer. NRSN2-AS1 can promote the expression of SOX12 and the malignant behavior of ovarian cancer cells in vitro.
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Objective To explore the relationship between the expression of DEAO-box helicase 5(DDX5) and transcription factor 12(TCF12) with amyotrophic lateral sclerosis ( ALS ) hippocampal lesions by detecting the expressions and the interaction of DDX5 and TCF12 in the hippocampus of SOD1-G93A mutant ALS transgenic mice. Methods Forty- two pairs of SOD1-G93A mutant ALS transgenic mice and wild-type mice were divided into three groups at the age of 95 days (early onset stage), 108 days (middle onset stage) and 122 days (late onset stage). RT-PCR, Western blotting and double immunofluorescence labeled technique were used to detect the expressions of DDX5 and TCF12 in the hippocampus. Co-immunoprecipitation assasy was used to detect the interaction between DDX5 and TCF12. Results Compared with the wild-type mice of the same age, DDX5 and TCF12 mRNA in the hippocampus of SOD1-G93A mutant ALS transgenic mice were unchanged, but DDX5 and TCF12 protein were up-regulated significantly at day 95, 108 and 122. DDX5 and TCF12 positive cells were found in both DG area and hippocampus proper, and DDX5 and TCF12 were co-localized with neurons. The immunoreactivities of DDX5 and TCF12 in the hippocampus of SOD1-G93A mutant transgenic mice were elevated compared with wild-type mice at the same time point. Co-immunoprecipitation assasys confirmed that there existed interactions between DDX5 and TCF12 protein. Conclusion DDX5 and TCF12 protein are up-regulated in the hippocampal tissues of SOD1-G93A mutant ALS transgenic mice. The abnormal expressions of DDX5 and TCF12 are involved in the hippocampal lesions of ALS.