ABSTRACT
The long noncoding RNA WEE2 antisense RNA 1 (WEE2-AS1) plays an oncogenic role in hepatocellular carcinoma and triple negative breast cancer progression. In this study, we investigated the expression and roles of WEE2-AS1 in glioblastoma (GBM). Furthermore, the molecular mechanisms behind the oncogenic actions of WEE2-AS1 in GBM cells were explored in detail. WEE2-AS1 expression was detected using quantitative real-time polymerase chain reaction. The roles of WEE2-AS1 in GBM cells were evaluated by the cell counting kit-8 assay, flow cytometric analysis, Transwell cell migration and invasion assays, and tumor xenograft experiments. WEE2-AS1 expression was evidently enhanced in GBM tissues and cell lines compared with their normal counterparts. An increased level of WEE2-AS1 was correlated with the average tumor diameter, Karnofsky Performance Scale score, and shorter overall survival among GBM patients. Functionally, depleted WEE2-AS1 attenuated GBM cell proliferation, migration, and invasion in vitro, promoted cell apoptosis, and impaired tumor growth in vivo. Mechanistically, WEE2-AS1 functioned as a molecular sponge for microRNA-520f-3p (miR-520f-3p) and consequently increased specificity protein 1 (SP1) expression in GBM cells. A series of recovery experiments revealed that the inhibition of miR-520f-3p and upregulation of SP1 could partially abrogate the influences of WEE2-AS1 downregulation on GBM cells. In conclusion, WEE2-AS1 can adsorb miR-520f-3p to increase endogenous SP1 expression, thereby facilitating the malignancy of GBM. Therefore, targeting the WEE2-AS1miR-520f-3pSP1 pathway might be a promising therapy for the management of GBM in the future.
Subject(s)
Cell Cycle Proteins/genetics , Glioblastoma/genetics , MicroRNAs/genetics , Protein-Tyrosine Kinases/genetics , RNA, Long Noncoding/genetics , Aged , Apoptosis/genetics , Carcinogenesis/genetics , Cell Cycle Proteins/metabolism , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Disease Progression , Down-Regulation , Female , Gene Expression Regulation, Neoplastic , Glioblastoma/pathology , Humans , Male , MicroRNAs/metabolism , Middle Aged , Neoplasm Invasiveness/genetics , Oncogenes , Protein-Tyrosine Kinases/metabolism , RNA, Antisense/genetics , RNA, Antisense/metabolism , RNA, Long Noncoding/metabolism , Sp1 Transcription Factor/metabolism , Xenograft Model Antitumor AssaysABSTRACT
OBJECTIVE: Idiopathic trigeminal neuralgia (ITN) can be effectively treated with radiofrequency thermocoagulation. However, this procedure requires cannulation of the foramen ovale, and conventional cannulation methods are associated with high failure rates. Multimodality imaging can improve the accuracy of cannulation because each imaging method can compensate for the drawbacks of the other. We aim to determine the feasibility and accuracy of percutaneous foramen ovale cannulation under the guidance of virtual navigation with multimodality image fusion in a self-designed anatomical model of human cadaveric heads. DESIGN: Five cadaveric head specimens were investigated in this study. Spiral computed tomography (CT) scanning clearly displayed the foramen ovale in all five specimens (10 foramina), which could not be visualized using two-dimensional ultrasound alone. The ultrasound and spiral CT images were fused, and percutaneous cannulation of the foramen ovale was performed under virtual navigation. After this, spiral CT scanning was immediately repeated to confirm the accuracy of the cannulation. RESULTS: Postprocedural spiral CT confirmed that the ultrasound and CT images had been successfully fused for all 10 foramina, which were accurately and successfully cannulated. The success rates of both image fusion and cannulation were 100%. CONCLUSIONS: Virtual navigation with multimodality image fusion can substantially facilitate foramen ovale cannulation and is worthy of clinical application.
Subject(s)
Catheterization , Foramen Ovale/surgery , Multimodal Imaging , Trigeminal Neuralgia/surgery , Catheter Ablation/methods , Catheterization/methods , Electrocoagulation/methods , Female , Foramen Ovale/diagnostic imaging , Humans , Male , Multimodal Imaging/methods , Tomography, X-Ray Computed/methods , Treatment OutcomeABSTRACT
OBJECTIVE: To explore the in vivo effects of myxoma virus (MV) on gliomas of rat model. Methods C6 glioma cells were implanted into the frontal lobe of SD rats using stereotactic methods to establish animal models of glioma. METHODS: C6 glioma cells were implanted into the frontal lobe of SD rats using stereotactic methods to establish animal models of glioma. Models were divided into 4 groups randomly after tumor growth was affirmed, and MV, 5-FU, MV + 5-FU, and denatured myxoma virus (DV) were implanted into the tumors using stereotactic methods, bodyweight, tumor size, expression of glial fibrillary acidic protein (GFAP), Akt of each model were observed. RESULTS: The gliomas in all SD rats were established successfully. And tumor growth in MV, 5-FU, MV + 5-FU were significantly decreased as compared with DV group after injection, sizes of some tumors were lessened, and GFAP expression decreased in MV, 5-FU and MV +5-FU groups. The expression of PI3k, Akt and mTOR were decreased in MV and MV +5-FU groups. CONCLUSION: C6 glioma SD rat models could be established successfully using stereotactic methods. MV may enhance biological activity of chemotherapeutic drugs on tumor cells of animal models in vivo by regulating some genes of PI3K-Akt-mTOR signal pathway.
Subject(s)
Brain Neoplasms/therapy , Glioma/therapy , Myxoma virus , Oncolytic Virotherapy , Animals , Disease Models, Animal , Female , Fluorouracil/therapeutic use , Male , Rats , Rats, Sprague-DawleyABSTRACT
OBJECTIVE: To evaluate the susceptibility of C6 glioma cells to Myxoma virus and the killing effect of Myxoma virus to the C6 glioma cells in vitro. METHODS: C6 glioma cells were infected with myxoma virus, used death virus as the negative control, 5-FU as the positive control, DEMD as blank control. The number of living cells were counted every 24 h, and Western-Blot method, inverted microscope and MTT assay were applicated to observe the cell morphology and survival rate in each group. RESULTS: The cell number were decreased rapidly in virus effected group and 5-FU group, with significant differences to the negative and blank control groups. And cells in virus effected group appeared cytopathic effect. CONCLUSIONS: C6 glioma cells were susceptible to myxoma virus and myxoma virus had killing effect to C6 glioma cells in vitro.
