LncRNA CASC19 promotes the proliferation, migration and invasion of non-small cell lung carcinoma via regulating miRNA-130b-3p.

OBJECTIVE: To uncover the biological role of long non-coding RNA (lncRNA) CASC19 in the pathogenesis of non-small cell lung carcinoma (NSCLC) and the potential mechanism. PATIENTS AND METHODS: Expression pattern of lncRNA CASC19 in NSCLC tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Survival analysis on the correlation between CASC19 level and prognosis of NSCLC patients was conducted by introducing for the Kaplan-Meier estimator. After the transfection of si-CASC19 in A549 and PC9 cells, changes in viability, migratory, and invasive capacities were evaluated. Dual-luciferase reporter gene assay was performed to explore the interaction between microRNA-130b-3p (miRNA-130b-3p) and CASC19/ZEB2. Their interactive effects on the progression of NSCLC were finally investigated through rescue experiments. RESULTS: LncRNA CASC19 was upregulated in NSCLC tissues and cell lines. NSCLC patients with high expression of CASC19 presented a worse survival. Knockdown of CASC19 attenuated proliferative, migratory, and invasive capacities of A549 and PC9 cells. CASC19 sponged miRNA-130b-3p and negatively regulated its level. ZEB2 was the direct target of miRNA-130b-3p. The knockdown of miRNA-130b-3p reversed the regulatory effects of CASC19 on A549 and PC9 cells. CONCLUSIONS: CASC19 sponges miRNA-130b-3p to regulate ZBR2 as a ceRNA, thus accelerating the progression of NSCLC by regulating proliferative, migratory, and invasive capacities of tumor cells.

Long-term monitoring of post-stroke plasticity after transient cerebral ischemia in mice using in vivo and ex vivo diffusion tensor MRI.

WE USED A MURINE MODEL OF TRANSIENT FOCAL CEREBRAL ISCHEMIA TO STUDY: 1) in vivo DTI long-term temporal evolution of the apparent diffusion coefficient (ADC) and diffusion fractional anisotropy (FA) at days 4, 10, 15 and 21 after stroke 2) ex vivo distribution of a plasticity-related protein (GAP-43) and its relationship with the ex vivo DTI characteristics of the striato-thalamic pathway (21 days). All animals recovered motor function. In vivo ADC within the infarct was significantly increased after stroke. In the stroke group, GAP-43 expression and FA values were significantly higher in the ipsilateral (IL) striatum and contralateral (CL) hippocampus compared to the shams. DTI tractography showed fiber trajectories connecting the CL striatum to the stroke region, where increased GAP43 and FA were observed and fiber tracts from the CL striatum terminating in the IL hippocampus.Our data demonstrate that DTI changes parallel histological remodeling and recovery of function.

Event-related auditory evoked potentials and multiple sclerosis.

Long latency event-related auditory evoked potentials, particularly the P300 wave, constitute an objective electrophysiological index of cognitive function. For this reason, these potentials have been studied in a series of 101 patients with multiple sclerosis (MS), classified according to McAlpine's criteria into definite, probable and possible cases. The patients were also classified as depressed or non-depressed according to the DSM-III and Research Diagnostic Criteria. They were also subjected to a battery of psychometric tests. In the patient population the N200 and P300 latencies were increased, as were the P200 latencies, when compared with a control population. This electrophysiological pattern had previously been observed in other conditions characterised by subcortical lesions. Partial correlations (at constant disease duration) between the disability score and the cognitive deficit were found to be significant. Patients with an increased P300 latency had a greater disability and the P300 latency was significantly correlated with the duration of the illness. The N200 and P300 latencies were increased in depressed MS subjects, but this increase did not reach the level of significance. Depression was more frequent in the more severely handicapped patients. This suggests that the origin of the depression seen in multiple sclerosis is only partly organic, and that it is one of the factors contributing to the subcortical cognitive deficit in multiple sclerosis. Progressive forms of the disease exhibited the most profound cognitive deficit, and the most marked increase in P300 latency.