Increasing evidence suggests that long non coding (lnc)RNA and microRNA (miRNA/miR) both regulate the expression of key genes in tumorigenesis and have considerable theranostic potential. Rapid advances in bioinformatics indicate that miRNA may potentially interact with lncRNA to modulate their regulatory roles. miR‑148b‑3p has been reported to have a vital role in regulating tumor progression. However, the expression pattern of miR‑148b‑3p in glioma remains largely unknown, and interactions between miR‑148b‑3p and lncRNA has yet to be identified. The aim of the present study was to insight into the regulatory role of miR‑148b‑3p in glioma. Using online software, the HOTAIR gene was identified as a possible lncRNA target of miR‑148b‑3p in the present study. siRNA was used to suppress the expression of HOTAIR and reverse transcription‑quantitative polymerase chain reaction was used to detect the expression of miR‑148b‑3p. The results confirmed that HOTAIR mRNA expression was inversely correlated with miR‑148b‑3p expression in A172 glioma cells. Furthermore, a 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay was performed to detect the viability of cells, flow cytometry was performed to test cell cycle and a matrigel invasion assay was performed to test cell invasion. The results showed that HOTAIR promotes factors associated with malignancy, including cell proliferation, cell cycle progression and invasion, whereas miR‑148b‑3p suppresses malignancy. Bioinformatics and luciferase reporter assays showed that miR‑148b‑3p modulates HOTAIR expression by directly targeting the HOTAIR gene sequence. In summary, the results indicated that miR‑148b‑3p inhibits malignant biological behaviors of glioma cells by directly targeting HOTAIR. The current data provide important evidence for understanding the key roles of the lncRNA miRNA functional network in glioma.

Although microvascular decompression (MVD) should be considered as the first‑line treatment for classic trigeminal neuralgia (TN) owing to neurovascular compression of the trigeminal nerve, an increasing number of surgeons prefer radiofrequency thermocoagulation (RFT). RFT is a Gasserian ganglion‑level ablative intervention that may achieve immediate pain relief for TN. It is used for emergency management when MVD is not suitable for the patient. As the gold surgical standard of classic trigeminal neuralgia, MVD has the advantage of longer efficacy. However, there are currently no high‑quality controlled trials to evaluate the efficacy of MVD and RFT. For the present systematic review, the PubMed, Embase and Cochrane databases (all entries up until July 31, 2020) were searched to identify studies related to RFT in order to provide valuable information for clinical decision‑making. The efficacy of the RFT method was evaluated in terms of the initial pain relief percentage, recurrence rate and follow‑up time. Furthermore, the incidence rate of various postoperative complications was retrieved. RFT was used for a wider range of applications than MVD, including use for primary (owing to neurovascular compression of the trigeminal nerve), idiopathic and secondary (due to primary neurological diseases) TN, and provided a high rate of initial pain relief and long‑term pain control. Although this method has several side effects, the incidence of complications could be reduced by precise cannulation. Furthermore, the complications that occurred were not permanent. Thus, RFT is a safe and effective minimally invasive method of pain relief for patients with TN.

The HOXB1 gene plays a critical role as an oncogene in diverse tumors. However, the functional role of HOXB1 and the mechanism regulating HOXB1 expression in glioma are not fully understood. A preliminary bioinformatics analysis showed that HOXB1 is ectopically expressed in glioma, and that HOXB1 is a possible target of miR-3175. In this study, we investigated the function of HOXB1 and the relationship between HOXB1 and miR-3175 in glioma. We show that HOXB1 expression is significantly downregulated in glioma tissues and cell lines, and that its expression may be closely associated with the degree of malignancy. Reduced HOXB1 expression promoted the proliferation and invasion of glioma cells, and inhibited their apoptosis in vitro, and the downregulation of HOXB1 was also associated with worse survival in glioma patients. More importantly, HOXB1 was shown experimentally to be a direct target of miR-3175 in this study. The downregulated expression of miR-3175 inhibited cell proliferation and invasion, and promoted apoptosis in glioma. The oncogenicity induced by low HOXB1 expression was prevented by an miR-3175 inhibitor in glioma cells. Our results suggest that HOXB1 functions as a tumor suppressor, regulated by miR-3175 in glioma. These results clarify the pathogenesis of glioma and offer a potential target for its treatment.

Objectives. The authors describe a technique that includes a stereotactic approach in the preoperative plan in cases where the foramen ovale is difficult to access for radiofrequency thermocoagulation of the Gasserian ganglion. Methods. The study included 395 patients for whom three-dimensional computed tomographic reconstruction of the skull base, maxilla, and mandible was conducted before surgery. Accessibility of the foramen ovale was defined using numerical data from the three-dimensional computed tomographic reconstruction images. In those patients for whom accessibility of the foramen ovale was considered difficult, the authors used a stereotactic frame to design an individual operative plan. Adjustments of a single point of data,—that is, a change in X axis, Y axis, or an arc angle—were guided by radiographic fluoroscopy images. After verifying successful cannulation and electroneurophysiology, thermocoagulation targets—especially multiple targets recorded as data on the Z axis of the stereotactic approach—were identified and treated. Results. There were 24 patients who met the predetermined criteria for having a difficult-to-access foramen ovales—that is, they had at least two contributing factors and/or involvement of division V1 . Twenty-one of the 24 patients required a single satisfactory puncture; three patients required two to three punctures to successfully access the foramen ovale. There were no permanent complications from the procedure. Conclusions. The authors conclude that this stereotactic approach combined with three-dimensional computed tomographic reconstruction model can improve the accuracy, safety, and efficiency of percutaneous radiofrequency thermocoagulation in patients with trigeminal neuralgia for whom the foramen ovale is difficult to access.

The roles of alternative splicing and RNA editing in gene regulation and transcriptome diversity are well documented. Adenosine deaminases acting on RNA (ADARs) are responsible for adenosine-to-inosine (A-to-I) editing and exemplify the complex association between RNA editing and alternative splicing. The self-editing activity of ADAR2, which acts on its own pre-mRNA, leads to its alternative splicing. Alternative splicing occurs independently at nine splicing sites on ADAR2 pre-mRNA, generating numerous alternative splicing variants with various catalytic activities. A-to-I RNA editing is important in a range of physiological processes in humans and is associated with several diseases, including amyotrophic lateral sclerosis, mood disorders, epilepsy and glioma. Reduced editing at the glutamine/arginine site of the AMPA receptor subunit GluA2 in glioma, without any alteration in ADAR2 expression, is a notable phenomenon. Several studies have tried to explain this alteration in the catalytic activity of ADAR2; however, the underlying mechanism remains unclear. The present review summarizes the relevant literature and shares experimental results concerning ADAR2 alternative splicing. In particular, the present review demonstrates that shifts in the relative abundance of the active and inactive splicing variants of ADAR2 may reduce the ADAR2 editing activity in glioma. Dominant expression of ADAR2 splicing variant with low enzyme activity causes reduced RNA editing of GluA2 subunit at the glutamine/arginine site in glioma.

RNA editing is catalyzed by adenosine deaminases acting on RNA (ADARs). ADAR2 is the main enzyme responsible for recoding editing in humans. Adenosine-to-inosine (A-to-I) editing at the Q/R site is reported to be decreased in gliomas; however, the expression of ADAR2 mRNA was not greatly affected.