Single-Center Analysis of Reliability of 3D-DSA Dual Volume Reconstruction for Evaluation of Endovascularly Treated Intracranial Aneurysms.

OBJECTIVE: To explore the applications of 3-dimensional digital subtraction angiography (3D-DSA) double-volume reconstruction technique (DVRT) in endovascular embolization for the treatment of intracranial aneurysm. METHODS: A cohort of 112 patients with a total of 127 intracranial aneurysms admitted to the neurosurgery department from June 2018 to October 2019 were selected. Cerebrovascular angiographies were performed after admission. Patients were divided into observation group (56 of 112) and control group (56 of 112) randomly when endovascular embolization was performed. Individuals in the control group were treated with 2D-DSA technique, and patients in the observation group were treated with 3D-DSA DVRT. The Raymond method was used to determine the degree of embolism. RESULTS: There was no significant difference in sex, blood pressure, cerebral atherosclerosis, aneurysm site or size, contrast agent dosage, x-ray dose, or surgical cost between the 2 groups. There was no postoperative recurrence in the observation group. However, the recurrence rate in the control group is 10.7% (6 of 56). Postoperative thrombosis occurred in 1 case (1 of 56, 1.8%) in the observation group and 7 cases (7 of 56, 12.5%) in the control group. No postoperative cerebral infarction was recorded in the observation group, while 5 cases (8.9%, 5 of 56) in the control group presented with postoperative cerebral infarction. CONCLUSIONS: 3D-DVRT for intracranial aneurysm embolization provides the best working angle, clearly shows the process of aneurysm embolization and its relationship with peripheral vessels, and reduces the occurrence of surgical complications including postoperative recurrence, thrombosis, and cerebral infarction.

Retracted Article: Overexpression of circ_0034642 contributes to hypoxia-induced glycolysis, cell proliferation, migration and invasion in gliomas by facilitating TAGLN2 expression via sponging miR-625-5p.

Glioma is an aggressive brain cancer with poor prognosis and high invasiveness. Dysregulation of circular RNAs (circRNAs) has been widely discovered in various cancers, including glioma. However, the molecular mechanism of circ_0034642 in glioma is still unclear. The expression of circ_0034642, microRNA (miR)-625-5p and transgelin-2 (TAGLN2) in glioma tumors and cells was detected by performing a quantitative real-time polymerase chain reaction (qRT-PCR). The stability of circ_0034642 was determined by carrying out RNase R treatment. Cell proliferation was evaluated by performing the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Glycolysis was analyzed by measuring the extracellular acidification rate (ECAR) using glucose detection and lactic acid detection kits. Cell migration and invasion were determined by performing the transwell assay. Protein expression levels of the proteins hexokinase 2 (HK2), matrix metalloproteinase-2 (MMP2), matrix metalloproteinase-9 (MMP9) and TAGLN2 were analyzed using western blots. The interaction between miR-625-5p and circ_0034642 or TAGLN2 was proved using a dual-luciferase reporter system. Animal models were established by subcutaneously injecting glioma cells stably transfected with sh-NC or sh-circ_0034642. Circ_0034642 and TAGLN2 were overexpressed whereas miR-625-5p was expressed at low levels in glioma tumors and cells. Moreover, circ_0034642 and TAGLN2 were upregulated while miR-625-5p was downregulated under hypoxic conditions in a time-dependent manner. Next, elimination of circ_0034642 was shown to inhibit cell glycolysis, proliferation, migration and invasion under hypoxic conditions in gliomas. Then, we found that circ_0034642 acted as a "sponge" of miR-625-5p while TAGLN2 acted as a target of miR-625-5p. In addition, recovery of circ_0034642 attenuated the repression mediated by miR-625-5p on glioma cell glycolysis and progression under hypoxic conditions. Meanwhile, an inhibitor of miR-625-5p alleviated TAGLN2 deficiency-induced inhibition of glioma cell development under hypoxic conditions. We also discovered that circ_0034642 could interact with miR-625-5p and further alter the expression of TAGLN2. Lastly, a circ_0034642 knockdown hindered tumor growth in vivo by regulating the miR-625-5p/TAGLN2 axis. Enhanced expression of circ_0034642 was found to promote cell glycolysis, proliferation, migration and invasion under hypoxic conditions in gliomas by sponging miR-625-5p to improve TAGLN2 expression, providing prospective biomarkers for the diagnosis of glioma.

Influence of Etoposide on anti-apoptotic and multidrug resistance-associated protein genes in CD133 positive U251 glioblastoma stem-like cells.

It has been hypothesized that cancer stem cell is responsible for the refractoriness of glioblastoma therapy. This study is to observe the influence of Etoposide on anti-apoptotic and multidrug resistance-associated protein genes in glioblastoma stem-like cells. U251 glioblastoma cells were cultured and CD133 positive cancer stem-like cells were isolated and identified. Cell counting kit-8 assay, cell morphology and flow cytometry were employed for assaying cell survival condition. Real-time quantitative PCR was chosen for detecting mRNA expression of livin, livinalpha, livinbeta, survivin, MRP1 and MRP3. As results, after Etoposide intervention, the U251 stem-like cells showed more resistant property, more intact morphology and lower apoptotic rate than that in U251 cells (p<0.05). It could be found that the expression of livinbeta in U251 stem-like cells was significantly higher (p<0.05). After Etoposide intervention, only livinalpha was suppressed markedly (p<0.05), while livin expression was not notably decreased with livinbeta increased on the contrary (p<0.05). MRP1 and MRP3 in U251 stem-like cells were significantly higher than that in cancer cells, and after chemotherapy, the expression of MRP1 increased notably (p<0.05). But the expression of survivin and MRP3 did not show these features. In conclusion, after Etoposide intervention glioblastoma stem-like cells showed a stronger resistance to apoptosis and death, and the anti-apoptotic gene livinbeta was more related with the high survival rate and MRP1 appeared to be more related with transporting chemotherapeutics out of glioblastoma stem-like cells.