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Background lncRNAs and VEGF have been shown to have close connections with oral squamous cell carcinoma (OSCC). We explored the interaction between lncRNA NEAT1 and VEGF-A in OSCC. Methods RT-qPCR was implemented to measure levels of lncRNA NEAT1 and VEGF-A in OSCC cell lines and normal cell lines. Cell functions then were checked after regulating the expressions of lncRNA NEAT1 and VEGF-A separately. Cell viabilities were examined with CCK-8 and apoptosis rate was checked with flow cytometry. Meanwhile, EMT-related genes E-cadherin, N-cadherin, Vimentin, and Snail and Notch signaling genes Notch1, Notch2, and Jagged were evaluated by RT-qPCR. IMR-1 was applied for impeding Notch signaling pathway. Later, cell viabilities, apoptosis, and EMT were assessed. Results Expressions of lncRNA NEAT1 and VEGF-A were both increased significantly in OSCC cell lines especially in TSCC1 cell line. Suppression of lncNRA NEAT1 was associated with lower cell viabilities and EMT and higher apoptosis rate in the TSCC1 cell line. Meanwhile, knockdown of VEGF-A significantly repressed cell viabilities and EMT in the TSCC1 cell line. Magnifying functions of inhibited lncRNA NEAT1 Notch signaling pathway was obviously activated with overexpressions of lncRNA NEAT1 and VEGF-A. Adding IMR-1 significantly downregulated cell viabilities and EMT and sharply increased apoptosis in the context of lncRNA NEAT1 and VEGF-A overexpression. Conclusion LncRNA NEAT1 may upregulate proliferation and EMT and repress apoptosis through activating VEGF-A and Notch signaling pathway in vitro, suggesting an underlying regulatory factor in OSCC. Nevertheless, further research is necessary to gain a greater understanding of lncRNA NEAT1 and connections with VEGF-A in vivo and in clinical study.

Periodontitis is a chronic inflammation caused by the deposition of dental plaque on the tooth surface. Human periodontal ligament stem cells (hPDLSCs) have the potential of osteogenic differentiation. Long non-coding RNAs (lncRNAs) are collectively involved in periodontitis. This study was designed to explore the roles of Linc01133 in osteogenic differentiation of hPDLSCs. hPDLSCs obtained from the periodontal ligament (PDL) of patients with periodontitis were used to collect Linc01133, microRNA-30c (miR-30c), and bone gamma-carboxyglutamate protein (BGLAP) expression data, and their expression changes were traced during osteogenic differentiation of hPDLSCs. Quantitative reverse-transcription polymerase chain reaction as well as western blotting were used to analyze the levels of RNAs and proteins. Dual-luciferase reporter and RNA pull-down assays demonstrated the relationship between Linc01133, miR-30c, and BGLAP. Furthermore, alkaline phosphatase (ALP) staining and alizarin red staining were applied to evaluate the degree of osteogenic differentiation. Linc01133 was downregulated in the PDL of patients with periodontitis. Upregulated Linc01133 promoted osteogenic differentiation of hPDLSCs. Linc01133 could inhibit miR-30c expression by sponging miR-30c. miR-30c suppressed osteogenic differentiation. Additionally, miR-30c targeted BGLAP. Knockdown of BGLAP abrogated the effects of decreased miR-30c on osteogenic differentiation of hPDLSCs. Linc01133 acted as a ceRNA to regulate osteogenic differentiation of hPDLSCs via the miR-30c/BGLAP axis. Therefore, Linc01133 may participate in the progress of periodontitis.

Background: Ginkgolide B (GB), the extract of G. biloba leaves, has been shown to be protective against many neurological disorders, including Parkinson's disease (PD). Efforts have been made to synthesized ginkgolides analogs and derivatives with more targeted and smaller molecular weight. In the present study, four GB derivatives (GBHC-1-GBHC-4) were synthesized, and their protective roles in N-methyl-4-phenylpyridinium (MPP +) injured MN9D dopaminergic neuronal cell line were evaluated. Also, cell response mechanisms upon these GB derivatives treatment were analyzed by iTRAQ proteomics. Methods: MN9D cells were treated with MPP + to induce in vitro cell models of PD. Four GB derivatives (GBHC-1-GBHC-4) were synthesized, and their protective roles on cell viability and apoptosis in in vitro PD model cells were evaluated by CCK8 assay, fluorescence-activated cell sorting and DAPI staining, respectively. The proteomic profiles of MPP+ injured MN9D cells pretreated with or without GB and GB derivatives were detected using the isobaric tags for relative and absolute quantification (iTRAQ) labeling technique. Results: Pretreatment with GBHC-1-GBHC-4 noticeably increased cell viability and attenuated cell apoptosis in MPP+-injured MN9D cells. Using proteomic analysis, we identified differentially expressed proteins upon GB and GB derivatives treatment. Chloride intracellular channel 4 (CLIC4) and "protein processing in endoplasmic reticulum" pathways participated in the protective roles of GB and GBHC-4. GB and GBHC-4 pretreatment could significantly reverse MPP+-induced CLIC4 expression and translocation from cytoplasm to nucleus of MN9D cells. Conclusions: Quantitative comparative proteomic analysis identified differentially expressed proteins associated with GB and GB derivatives. We further verified the expression of CLIC4 by western blotting and immunocytochemistry assay. This bio-information on the identified pathways and differentially expressed proteins such as CLIC4 provide more targeted directions for the synthesis of more effective and targeted GB derivatives for the treatment of neurological disorders.