Background: LncRNA NEAT1 has been identified as a tumour driver in many human cancers. However, the underlying mechanism of lncRNA NEAT1 in diffuse large B-cell lymphoma (DLBCL) progression is unclear.
Methods:The expression levels of NEAT1, GLI1 and miR-34b-5p were detected by RT-qPCR and Western blotting in DLBCL tissues and cell lines. MTT and colony formation assays were performed to examine cell proliferation, while annexin-V staining and TUNEL assays were performed to measure cell apoptosis. The effect of NEAT1, GLI1 and miR-34b-5p on cell cycle-associated proteins was evaluated by Western blotting. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were employed to investigate the interaction between NEAT1 and miR-34b-5p or GLI1 and miR-34b-5p. Moreover, chromatin immunoprecipitation (ChIP) was performed to demonstrate the interaction between MYC and NEAT1.Results: NEAT1 and GLI1 were upregulated while miR-34b-5p was downregulated in DLBCL tissues and cell lines compared to normal controls. Knockdown of NEAT1 or overexpression of miR-34b-5p inhibited cell proliferation but promoted cell apoptosis. Overexpression of NEAT1 reversed GLI1-knockdown induced attenuation of cell proliferation. In other words, NEAT1 acted as a competing endogenous RNA (ceRNA), regulating the miR-34b-5p-GLI1 axis, further affecting the proliferation of DLBCL. Moreover, MYC modulated NEAT1 transcription by directly binding to the NEAT1 promoter.
Conclusion:We revealed that MYC-regulated NEAT1 promoted DLBCL proliferation via the miR-34b-5p-GLI1 pathway, which could provide a novel therapeutic target for DLBCL.
Con OA+PA OA+PA+V100 OA+PA+V200 Effect of vascular endothelial growth factor B (VEGFB) on C2C12 myotube lipid accumulation. After 5 days of cell differentiation, cells were cultured in serum-free high-glucose DMEM after starvation, then with 100 μM oleic acid (OA) and 50 μM palmitic acid (PA) and different concentrations of VEGFB186 for 24 h. Oil-red O (ORO) staining (200x); Supplementary 2:C2C12 cells VEGFR1 expression.After 5 days of cell differentiation, cells were collected. VEGFR1 protein expression.
A highly efficient and convenient Barbier‐Grignard‐type reaction to give salicyl alcohols and novel facile protocol to furnish unsymmetrical 9‐arylxanthenes using sodium salicylates and unactivated bromo‐hydrocarbons are described. Of total 21 synthesized compounds, 18 compounds containing 14 alcohols and 4 9‐arylxanthenes are new compounds. The products were provided in yields among 38–99%. The electronic and steric effects of bromo‐hydrocarbons on the reaction were discussed. Based on experimental results, a plausible mechanism concerning direct formation of salicyl alcohol from salicylate and PhMgBr with the promotion of PPh3 is proposed.
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