Long noncoding RNA(lncRNA)IDH1 antisense RNA 1(IDH1-AS1)is involved in the progression of multiple cancers,but its role in epithelial ovarian cancer(EOC)is unknown.Therefore,we investigated the expression levels of ID...Long noncoding RNA(lncRNA)IDH1 antisense RNA 1(IDH1-AS1)is involved in the progression of multiple cancers,but its role in epithelial ovarian cancer(EOC)is unknown.Therefore,we investigated the expression levels of IDH1-AS1 in EOC cells and normal ovarian epithelial cells by quantitative real-time PCR(qPCR).We first evaluated the effects of IDH1-AS1 on the proliferation,migration,and invasion of EOC cells through cell counting kit-8,colony formation,EdU,transwell,wound-healing,and xenograft assays.We then explored the downstream targets of IDH1-AS1 and verified the results by a dual-luciferase reporter,qPCR,rescue experiments,and Western blotting.We found that the expression levels of IDH1-AS1 were lower in EOC cells than in normal ovarian epithelial cells.High IDH1-AS1 expression of EOC patients from the Gene Expression Profiling Interactive Analysis database indicated a favorable prognosis,because IDH1-AS1 inhibited cell proliferation and xenograft tumor growth of EOC.IDH1-AS1 sponged miR-518c-5p whose overexpression promoted EOC cell proliferation.The miR-518c-5p mimic also reversed the proliferation-inhibiting effect induced by IDH1-AS1 overexpression.Furthermore,we found that RNA binding motif protein 47(RBM47)was the downstream target of miR-518c-5p,that upregulation of RBM47 inhibited EOC cell proliferation,and that RBM47 overexpressing plasmid counteracted the proliferation-promoting effect caused by the IDH1-AS1 knockdown.Taken together,IDH1-AS1 may suppress EOC cell proliferation and tumor growth via the miR-518c-5p/RBM47 axis.展开更多
目的探讨miR-200c-5p对人结直肠癌细胞系SW480恶性增殖的影响。方法将miR-200c-5p模拟物/抑制剂及阴性对照分别瞬时转染人结直肠癌细胞系SW480。通过qPCR检测miR-200c-5p的表达,利用CCK-8法和平板克隆形成试验检测miR-200c-5p对结直肠...目的探讨miR-200c-5p对人结直肠癌细胞系SW480恶性增殖的影响。方法将miR-200c-5p模拟物/抑制剂及阴性对照分别瞬时转染人结直肠癌细胞系SW480。通过qPCR检测miR-200c-5p的表达,利用CCK-8法和平板克隆形成试验检测miR-200c-5p对结直肠癌细胞增殖活力和克隆形成能力的影响。使用生物信息学方法分析miR-200c-5p在结直肠癌中的差异靶基因和相关通路。结果瞬时转染miR-200c-5p模拟物/抑制剂成功高/低表达miR-200c-5p(P<0.05);高表达miR-200c-5p细胞增殖活力降低,低表达则相反(P<0.05);高表达miR-200c-5p的细胞克隆形成率低于对照组细胞,低表达则相反(P<0.05);miR-200c-5p的靶基因CXCL10在结直肠癌细胞中显著上调,C2orf72、ZC3H12C和DST显著下调,miR-200c-5p显著相关的KEGG通路为“melanoma”、“microRNAs in cancer”和“bladder cancer”。结论miR-200c-5p抑制人结直肠癌细胞系SW480的增殖及克隆形成,与结直肠癌的发生、发展相关。展开更多
基金supported by the National Natural Science Foundation of China(Grant Nos.81572556 and 81402139).
文摘Long noncoding RNA(lncRNA)IDH1 antisense RNA 1(IDH1-AS1)is involved in the progression of multiple cancers,but its role in epithelial ovarian cancer(EOC)is unknown.Therefore,we investigated the expression levels of IDH1-AS1 in EOC cells and normal ovarian epithelial cells by quantitative real-time PCR(qPCR).We first evaluated the effects of IDH1-AS1 on the proliferation,migration,and invasion of EOC cells through cell counting kit-8,colony formation,EdU,transwell,wound-healing,and xenograft assays.We then explored the downstream targets of IDH1-AS1 and verified the results by a dual-luciferase reporter,qPCR,rescue experiments,and Western blotting.We found that the expression levels of IDH1-AS1 were lower in EOC cells than in normal ovarian epithelial cells.High IDH1-AS1 expression of EOC patients from the Gene Expression Profiling Interactive Analysis database indicated a favorable prognosis,because IDH1-AS1 inhibited cell proliferation and xenograft tumor growth of EOC.IDH1-AS1 sponged miR-518c-5p whose overexpression promoted EOC cell proliferation.The miR-518c-5p mimic also reversed the proliferation-inhibiting effect induced by IDH1-AS1 overexpression.Furthermore,we found that RNA binding motif protein 47(RBM47)was the downstream target of miR-518c-5p,that upregulation of RBM47 inhibited EOC cell proliferation,and that RBM47 overexpressing plasmid counteracted the proliferation-promoting effect caused by the IDH1-AS1 knockdown.Taken together,IDH1-AS1 may suppress EOC cell proliferation and tumor growth via the miR-518c-5p/RBM47 axis.
文摘目的探讨miR-200c-5p对人结直肠癌细胞系SW480恶性增殖的影响。方法将miR-200c-5p模拟物/抑制剂及阴性对照分别瞬时转染人结直肠癌细胞系SW480。通过qPCR检测miR-200c-5p的表达,利用CCK-8法和平板克隆形成试验检测miR-200c-5p对结直肠癌细胞增殖活力和克隆形成能力的影响。使用生物信息学方法分析miR-200c-5p在结直肠癌中的差异靶基因和相关通路。结果瞬时转染miR-200c-5p模拟物/抑制剂成功高/低表达miR-200c-5p(P<0.05);高表达miR-200c-5p细胞增殖活力降低,低表达则相反(P<0.05);高表达miR-200c-5p的细胞克隆形成率低于对照组细胞,低表达则相反(P<0.05);miR-200c-5p的靶基因CXCL10在结直肠癌细胞中显著上调,C2orf72、ZC3H12C和DST显著下调,miR-200c-5p显著相关的KEGG通路为“melanoma”、“microRNAs in cancer”和“bladder cancer”。结论miR-200c-5p抑制人结直肠癌细胞系SW480的增殖及克隆形成,与结直肠癌的发生、发展相关。
