Chemokine receptor 7 (CCR7) has emerged as an inducer of invasion, migration, and epithelial-mesenchymal transition (EMT) in cancer. In this research, human malignant glioma cells were stimulated with transforming growth factor beta 1 (TGF-β1) and siCCR7. The data show that CCR7 mediates TGF-β1-induced EMT, migration, and invasion in U251 and U87 cells and that these effects of TGF-β1 were reversed by treatment with siCCR7 or a CCR7 neutralizing antibody. Importantly, the TGF-β1-mediated increase in nuclear factor kappaB (NF-κB) activity in human glioma cells was reduced by treatment with siCCR7 or a CCR7 neutralizing antibody. Furthermore, CCR7 was shown to mediate TGF-β1-induced glioma cancer cell migration by activating matrix metalloproteinase 2 (MMP2)/9. Our results indicate that CCR7 mediates TGF-β1-induced MMP2/9 expression through NF-κB signaling, thus facilitating glioma cell migration, invasion, and EMT, all of which progressively increase with glioblastoma progression. These findings indicate that CCR7 is a potential therapeutic target for malignant glioma.

Epilepsy is a common complex neurological disorder, and some forms are resistant to drug treatment. The HCN1/HCN2 genes encode hyperpolarization-activated cyclic nucleotide-gated channels, which play important roles in the electrophysiology of neurons. We investigated the association between HCN1/HCN2 variants and drug resistance or the risk of genetic generalized epilepsies (GGEs). We used matrix-assisted laser desorption/ionization time-of-flight mass spectrometry to assess nine variants of HCN1/HCN2 in 284 healthy participants and 483 GGEs (279 drug-responsive, 204 drug-resistant). Frequencies of HCN2 rs7255568 and rs3752158 G alleles differed in GGEs and in controls (P = .039, P = .027, respectively). The frequency of HCN2 haplotype (CAC) was higher in patients than controls (P = .046). The frequency of the HCN1 rs10462087 CC+CT genotype was lower in patients with childhood absence epilepsy (CAE) than controls (P = .047). Rs7255568 was associated with the risk of CAE (P = .028) and juvenile myoclonic epilepsy (JME) (P = .02). Rs3752158 was associated with the risk of generalized tonic-clonic seizures, JME, and febrile seizures (all P < .05). The frequency of the HCN2 haplotype (CAC) was higher in patients with JME (P = .015) and in those with febrile seizures (P = .024) than in controls. No significant association was found between HCN1/HCN2 alleles, genotypes or haplotypes, and drug resistance in patients. After Bonferroni's multiple comparisons correction, only the HCN2 rs3752158 C allele and GC+CC genotype frequencies in patients with JME were higher than those in controls (19.2% vs 11.6%, odds ratio (OR) = 1.71, 95% CI = 1.18-2.32), P = .004 < 0.05/9; 36% vs 22.2%, OR = 1.62(1.18-2.23), P = .003 < 0.05/9). Our study suggests that HCN2 rs3752158 is involved in the susceptibility to JME.

Background: Long noncoding RNAs (lncRNA) exert essential functions during tumorigenesis. However, how lncRNAs participate in glioma development remains poorly researched. This study aimed to determine how DDX11-AS1 affects glioma progression. Methods: Gene expression was analyzed by qRT-PCR. Survival rate curve was plotted in 56 glioma patients. Loss-of-function assays were performed to analyze proliferation, migration, and invasion through CCK8, colony formation, and transwell assays. Luciferase assay and RNA pulldown assays were conducted to illustrate the underlying molecular mechanism. Results: DDX11-AS1 expression was upregulated in glioma tissues and cells. DDX11-AS1 overexpression was linked with poor prognostic value. DDX11-AS1 knockdown suppressed proliferation, migration, and invasion while inducing apoptosis. DDX11-AS1 interacted with miR-499b-5p to eliminate it, leading to upregulation of RWDD4 expression. RWDD4 was upregulated in glioma while miR-499b-5p was downregulated. Conclusion: DDX11-AS1 upregulation promotes glioma progression through acting as a competing endogenous RNA for miR-499b-5p to upregulate RWDD4.

The supine roll maneuver is mainly for diagnosis of lateral semicircular canal BPPV. The Modified Dix-Hallpike maneuver is more specific for the diagnosis of posterior semicircular canal BPPV. The side-lying bow maneuver designed here is theoretically suitable for diagnosis of anterior semicircular canal BPPV.