Effects of LncRNA-ATB on human peritoneal mesothelial cells phenotypic transition and proliferation induced by high glucose / 解放军医学杂志

Objective To explore the effect of long noncoding RNA-ATB (LncRNA-ATB) on phenotypic transition and proliferation of human peritoneal mesothelial cells (HPMCs) induced by high glucose.Methods HPMCs used in experiment were divided into three groups:control group,mannitol group and hypertonic glucose group.HPMCs in control group received no treatment,and in hypertonic glucose group and mannitol group were treated with 50mmol/L D-glucose and isotonic mannitol for 72 hours,respectively.Real-time PCR was employed to detect the mRNA expression of LncRNA-ATB,E-cadherin,α-smooth muscle actin (α-SMA),connective tissue growth factor (CTGF),Cyclin D1,cyclin dependent kinase inhibitor 4 (CDK4),protein 27 (p27)and proliferating cell nuclear antigen (PCNA).Western blotting was performed to detect the proteins expression of E-cadherin,α-SMA,CTGF,Cyclin D1,CDK4,p27 and PCNA,and flow cytometry was used to test the cell cycle.Lentivirus artifice was used to up-or down-regulate the expression of LncRNA-ATB in untreated HPMCs.Real-time PCR was employed to detect the mRNA expression of E-cadherin,α-SMA and CTGF,Western blotting was performed to detect the proteins expression of E-cadherin,α-SMA and CTGF,and flow cytometry was used to test the cell cycle.Results It is revealed by Real-time PCR,Western blotting and flow cytometry that the expressions increased of LncRNA-ATB,α-SMA,CTGF,Cyclin D1,CDK4 and PCNA induced by hypertonic glucose,and decreased of E-cadherin and p27 (P＜0.05).Up-regulation of LncRNA-ATB promoted HPMCs phenotypic transition and proliferation,while down-regulation alleviated HPMCs phenotypic transition and proliferation.Conclusion Hypertonic glucose may accelerate HPMCs phenotypic transition and proliferation by up-regulating the expression of LncRNA-ATB.

[Effects of decitabine on biological behavior of U266 cells].

This study was aimed to explore the effects of decitabine on the biological behaviour of U266 cells in vitro so as to provide a new thinking and experiment basis, as well as new evidences for the pathogenesis of multiple myeloma. MTT and colony formation assays were used to evaluate the impact of decitabine on the ability of proliferation of U266 cells; flow cytometry was used to analyze the cell distribution in cell cycle; transwell chamber and matrigel assays were used to observe the ability of migration and invasion. The results indicated that decitabine could significantly suppress the proliferation of U266 cells in time-and dose-dependent manners. The flow cytometric analysis demonstrated that the cells in G(0)-G(1) phase significantly increased while the cells in S and G(2)/M phase decreased. The migration and matrigel invading tests showed that the number of cells moving into under chamber of transwell decreased after U266 cells treated with decitabine. It is concluded that decitabine may act as an effective drug for MM by inhibiting the proliferation, migration and invasion ability, and the specific mechanism needs to be deeply explored.