LncRNA MIR17HG promotes the proliferation, migration, and invasion of retinoblastoma cells by up-regulating HIF-1α expression via sponging miR-155-5p.

Long non-coding RNA (lncRNA) miR-17-92a-1 cluster host gene (MIR17HG) is oncogenic in several cancers. This study was aimed to probe into its expression characteristics and biological functions in retinoblastoma (RB) and to explore its role in regulating microRNA-155-5p (miR-155-5p) and hypoxia-inducible factor-1α (HIF-1α). In this study, paired RB samples were collected, and expression levels of MIR17HG, miR-155-5p, and HIF-1α were examined by quantitative real-time polymerase chain reaction (qRT-PCR); the proliferation, migration, and invasion of RB cells were detected by cell counting kit-8 (CCK-8) and transwell assays; qRT-PCR and Western blot were used to analyze the changes of miR-155-5p expression and HIF-1α expression. We found that MIR17HG expression was significantly up-regulated in RB samples, which was negatively correlated with miR-155-5p expression. The proliferation, migration, and invasion of RB cells were promoted by MIR17HG overexpression but inhibited by MIR17HG knockdown. MiR-155-5p suppressed the proliferation, migration, and invasion of RB cells. MIR17HG positively regulated the expression of HIF-1α on both mRNA and protein levels in RB cells. Additionally, miR-155-5p was identified as a target of MIR17HG. The data in this study suggest that MIR17HG exerts oncogenic effects in RB via the miR-155-5p/HIF-1α axis.

[Effect of bicuculline on first spike latency of the neurons in the inferior colliculus of mice].

OBJECTIVE: To evaluate the effect of bicuculline on the first spike latency of the neurons in the inferior colliculus of mice and investigate the role of GABA inhibition in sound signal processing of the neurons. METHODS: In vivo extracellular recording was performed on the inferior colliculus of 13 BALB/c mice (4 to 5 weeks old) to record the neuronal response to pure tones. Bicuculline, a GABA-A receptor antagonist, was applied to the neurons iontophoretically through one channel in the three-barrel glass-pipettes. The first spike latency and other response properties of the characteristic frequency were recorded for analysis. RESULTS: A total of 30 well-isolated single neurons were recorded. Increased spike counts characterized 96% of the neurons, with either increased (40%) or decreased (60%) latency of neuronal responses. Characteristic frequency alterations occurred in 50% of the neurons with increased spike latency, and the minimum threshold showed linear changes. CONCLUSION: GABAergic inhibition may participate in the latency formation and increased frequency selectivity of mouse inferior colliculus neurons by lateral inhibition. The changes in the first spike latency can be indicative of the information integration in GABAergic neurons at the synaptic level.

Immunohistochemical investigation of voltage-gated potassium channel-interacting protein 1 in normal rat brain and Pentylenettrazole-induced seizures.

Objective To explore the possible role of voltage-gated potassium channel-interacting protein 1 (KChIP1) in the pathogenesis of epilepsy. Methods Sprague Dawley female adult rats were treated with pentylenettrazole (PTZ) to develop acute and chronic epilepsy models. The approximate coronal sections of normal and epilepsy rat brain were processed for immunohistochemistry. Double-labeling confocal microscopy was used to determine the coexistence of KChIP1 and gamma-aminobutyric acid (GABA). Results KChIP1 was expressed abundantly throughout adult rat brain. KChIP1 is highly co-localize with GABA transmitter in hippocampus and cerebral cortex. In the acute PTZ-induced convulsive rats, the number of KChIP1-postive cells was significantly increased especially in the regions of CA1 and CA3 (P < 0.05); whereas the chronic PTZ-induced convulsive rats were found no changes. The number of GABA-labeled and co-labeled neurons in the hippocampus appeared to have no significant alteration responding to the epilepsy-genesis treatments. Conclusion KChIP1 might be involved in the PTZ-induced epileptogenesis process as a regulator to neuronal excitability through influencing the properties of potassium channels. KChIP1 is preferentially expressed in GABAergic neurons, but its changes did not couple with GABA in the epileptic models.