Table_3_Microarray analysis of lncRNA and mRNA expression profiles in patients with Legg-Calve-Perthes disease.XLSX

BackgroundThe etiology and underlying pathogenic mechanisms of Legg-Calve-Perthes disease (LCPD) still remain unclear. A disruption of blood supply to the femoral head, producing ischemic necrosis, appears to be the critical pathological event. The lncRNAs play crucial roles in many biological processes and are dysregulated in various human diseases. However, its expression profiles and the potential regulatory roles in the development of LCPD have not been investigated.MethodsIn this study, differentially expressed lncRNA and mRNA of Legg-Calve-Perthes disease patients were profiled. Several GO terms and pathways that play important roles in the regulation of vascular structure, function or coagulation were selected for further analysis. The lncRNA -mRNA interacting networks in LCPD tissues were constructed to identify novel potential targets for further investigation.ResultsThe microarray analysis revealed that 149 lncRNAs and 37 mRNAs were up-regulated, and 64 lncRNAs and 250 mRNAs were down-regulated in LCPD tissues. After filtering, we finally found 14 mRNAs and constructed an mRNA-lncRNA interacting network. Through the analysis of the interaction network, we finally found 13 differentially expressed lncRNAs, which may be implicated in the pathogenesis of LCPD. These mRNAs/lncRNAs were further validated with qRT-PCR.ConclusionThe findings of this study established a co-expression network of disease-related lncRNAs and mRNAs which screened out from the concerned G.O. terms and Pathways, which may provide new sights for future studies on molecular mechanisms of LCPD.</p

Table_2_Microarray analysis of lncRNA and mRNA expression profiles in patients with Legg-Calve-Perthes disease.XLSX

BackgroundThe etiology and underlying pathogenic mechanisms of Legg-Calve-Perthes disease (LCPD) still remain unclear. A disruption of blood supply to the femoral head, producing ischemic necrosis, appears to be the critical pathological event. The lncRNAs play crucial roles in many biological processes and are dysregulated in various human diseases. However, its expression profiles and the potential regulatory roles in the development of LCPD have not been investigated.MethodsIn this study, differentially expressed lncRNA and mRNA of Legg-Calve-Perthes disease patients were profiled. Several GO terms and pathways that play important roles in the regulation of vascular structure, function or coagulation were selected for further analysis. The lncRNA -mRNA interacting networks in LCPD tissues were constructed to identify novel potential targets for further investigation.ResultsThe microarray analysis revealed that 149 lncRNAs and 37 mRNAs were up-regulated, and 64 lncRNAs and 250 mRNAs were down-regulated in LCPD tissues. After filtering, we finally found 14 mRNAs and constructed an mRNA-lncRNA interacting network. Through the analysis of the interaction network, we finally found 13 differentially expressed lncRNAs, which may be implicated in the pathogenesis of LCPD. These mRNAs/lncRNAs were further validated with qRT-PCR.ConclusionThe findings of this study established a co-expression network of disease-related lncRNAs and mRNAs which screened out from the concerned G.O. terms and Pathways, which may provide new sights for future studies on molecular mechanisms of LCPD.</p

Table_1_Microarray analysis of lncRNA and mRNA expression profiles in patients with Legg-Calve-Perthes disease.XLSX

BackgroundThe etiology and underlying pathogenic mechanisms of Legg-Calve-Perthes disease (LCPD) still remain unclear. A disruption of blood supply to the femoral head, producing ischemic necrosis, appears to be the critical pathological event. The lncRNAs play crucial roles in many biological processes and are dysregulated in various human diseases. However, its expression profiles and the potential regulatory roles in the development of LCPD have not been investigated.MethodsIn this study, differentially expressed lncRNA and mRNA of Legg-Calve-Perthes disease patients were profiled. Several GO terms and pathways that play important roles in the regulation of vascular structure, function or coagulation were selected for further analysis. The lncRNA -mRNA interacting networks in LCPD tissues were constructed to identify novel potential targets for further investigation.ResultsThe microarray analysis revealed that 149 lncRNAs and 37 mRNAs were up-regulated, and 64 lncRNAs and 250 mRNAs were down-regulated in LCPD tissues. After filtering, we finally found 14 mRNAs and constructed an mRNA-lncRNA interacting network. Through the analysis of the interaction network, we finally found 13 differentially expressed lncRNAs, which may be implicated in the pathogenesis of LCPD. These mRNAs/lncRNAs were further validated with qRT-PCR.ConclusionThe findings of this study established a co-expression network of disease-related lncRNAs and mRNAs which screened out from the concerned G.O. terms and Pathways, which may provide new sights for future studies on molecular mechanisms of LCPD.</p

Additional file 4 of Circular RNA circEMB promotes osteosarcoma progression and metastasis by sponging miR-3184-5p and regulating EGFR expression

Additional file 4: Fig. S3. Overexpression of miR-3184-5p was associated with decreased OSA cell migration and invasion, nor increased apoptosis and G1/S phase arrest. (A-B) The proliferation ability of OSA cells after overexpression of miR-3184-5p was determined by CCK-8. (C-F) Transwell assays detected the changes of invasion and metastasis ability of OSA cells with or without miR-3184-5p overexpression. (C and E) Refer to 143B, while (D and F) refer to U2OS. Scale bar, 100 μm. (G-H) Flow cytometric apoptosis analysis detected the changes of apoptosis of OSA cells with or without miR-3184-5p overexpression. (I-K) Flow cytometry assay showed the regulation of cell cycle by overexpressing miR-3184-5p. Data are expressed as mean ± SD (n = 3) (*, p < 0.05; **, p < 0.01; ***, p < 0.001)

Additional file 2 of Circular RNA circEMB promotes osteosarcoma progression and metastasis by sponging miR-3184-5p and regulating EGFR expression

Additional file 2: Fig. S1. Verification of transfection efficiency of miR-3184-5p in OSA cells. (A) After the transfection of mimic and inhibitor of miR-3184-5p, qRT-PCR was used to detect the transfection efficiencies. Data are expressed as mean ± SD (n = 3) (*, p < 0.05; **, p < 0.01; ***, p < 0.001)

Additional file 1 of Circular RNA circEMB promotes osteosarcoma progression and metastasis by sponging miR-3184-5p and regulating EGFR expression

Additional file 1: Table S1. Primer sequences for qRT-PCR in this study

Additional file 3 of Circular RNA circEMB promotes osteosarcoma progression and metastasis by sponging miR-3184-5p and regulating EGFR expression

Additional file 3: Fig. S2. The relationship between the miR-3184-5p and clinicopathological characteristics. (A) Comparison of miR-3184-5p expression between non-metastatic and metastatic OSA tissues. (B) Distribution characteristics of miR-3184-5p expression in the TNM stage of OSA. (C) In the 53-patients cohort, according to the median value of miR-3184-5p expression, they were divided into high expression group and low expression group. (D) Overall survival analysis of patients with low and high expression of miR-3184-5p using log-rank test and Kaplan–Meier analysis. (E) Correlation analysis between circEMB and miR-3184-5p in OSA tissues. (F) Relative miR-3184-5p levels in OSA cell lines and normal osteoblasts were ascertained by qRT-PCR. Data are expressed as mean ± SD (n = 3) (*, p < 0.05; **, p < 0.01; ***, p < 0.001)