LncRNA GAS5 Modulates the Progression of Glioma Through Repressing miR-135b-5p and Upregulating APC.

Purpose: The main purpose of this paper is to explore the interaction between GAS5 and miR-135b-5p to understand their function in the metastasis, invasion, and proliferation of glioma. This may provide new ideas for the pathogenesis and treatment of glioma. Patients and Methods: Western blotting assays and RT­qPCR were employed to investigate the expression of related genes in glioma tissues or cell lines. CCK-8 was used to examine the impact of GAS5 on cell viability. Motile activities were adopted by the transwell and wound healing experiments. A double luciferase experiment was performed to elucidate transcriptional regulation. Results: GAS5 showed low expression in glioma cells and tissues, and up-regulation of GAS5 could depress the invasion, proliferation, and metastasis of glioma. GAS5 negatively regulates miR-135b-5p, which can counteract the cellular effects caused by GAS5. APC was the target of miR-135b-5p, and GAS5 can regulate the expression of APC by sponging miR-135b-5p. APC overexpression reversed the effects of miR-135b-5p promotion on glioma cells, while miR-135b-5p has the opposite function. As a downstream target gene of GAS5, miR-135b-5p was negatively regulated by GAS5. The restoration of miR-135b-5p can remarkably reverse the impact of GAS5 on glioma cells. In addition, GAS5 increased the expression of APC in glioma cells by inhibiting miR-135b-5p. Conclusion: GAS5 increased APC expression by restraining miR-135b-5p and partially blocked the progression of glioma, suggesting that it could be an advantageous therapeutic target for glioma intervention.

Outcomes and risk factors for failure of trabeculectomy in glaucomatous patients in Southwest China: a 325 eyes analysis.

AIM: To evaluate the outcomes and elucidate the failure factors for trabeculectomy with mitomycin C (MMC) in Southwest Chinese patients. METHODS: A retrospective correlational study was conducted on the glaucomatous patients who underwent initial trabeculectomy with MMC in Southwest Hospital and had been followed up for 1-3y. A complete success for surgery is defined as a postoperative intraocular pressure (IOP) >5 and ≤21 mm Hg and 20% reduction of IOP compared to preoperative, without IOP-lowering medications. A qualified success for surgery is defined as the abovementioned postoperative IOP with or without IOP-lowering medications. The primary outcomes were IOP, the number of IOP-lowering medications, and cumulative success rate. The secondary outcomes included best corrected visual acuity (BCVA), mean deviation (MD) of visual field, major complications, and risk factors for surgical failure. RESULTS: A total of 325 eyes of 261 glaucomatous patients had been included in our study. Both the mean IOP and the number of IOP-lowering medications were significantly decreased from 32.9±12.0 to 16.4±5.7 mm Hg (P<0.0001) and 3.0±0.9 to 0.9±1.0 (P<0.0001), respectively, at the last visit. The cumulative complete success rate and qualified success rate were 77.8% and 92.0% at 1-year follow-up, and 47.2% and 77.7% at 3-year follow up. There were no significant differences in surgical outcomes between primary angle-closure glaucoma (PACG) and primary open angle glaucoma (POAG). In PACG patients, the success rates of trabeculectomy were comparable with those of phacotrabeculectomy. Hypertension (HR=1.904, P=0.011), encapsulated bleb (HR=2.756, P<0.001), and more preoperative topical medications (HR=2.475, P=0.008) were risk factors for surgical failure. CONCLUSION: The qualified success rate of trabeculectomy with MMC in glaucomatous patients in the cohort is 92.0% at 1-year, and 77.7% at 3-year follow up. Hypertension, encapsulated bleb, and more preoperative topical medications are associated with surgical failure.

Downregulation of TET1 Promotes Glioma Cell Proliferation and Invasion by Targeting Wnt/ß-Catenin Pathway.

Glioma is the most common malignant tumor in adult brain characteristic with poor prognosis and low survival rate. Despite the application of advanced surgery, chemotherapy, and radiotherapy, the patients with glioma suffer poor treatment effects due to the complex molecular mechanisms of pathological process. In this paper, we conducted the experiments to prove the critical roles TET1 played in glioma and explored the downstream targets of TET1 in order to provide a novel theoretical basis for clinical glioma therapy. RT-qPCR was adopted to detect the RNA level of TET1 and ß-catenin; Western blot was taken to determine the expression of proteins. CCK8 assay was used to detect the proliferation of glioma cells. Flow cytometry was used to test cell apoptosis and distribution of cell cycle. To detect the migration and invasion of glioma cells, wound healing assay and Transwell were performed. It was found that downregulation of TET1 could promote the proliferation migration and invasion of glioma cells and the concomitant upregulation of ß-catenin, and its downstream targets like cyclinD1 and c-myc were observed. The further rescue experiments were performed, wherein downregulation of ß-catenin markedly decreases glioma cell proliferation in vitro and in vivo. This study confirmed the tumor suppressive function of TET1 and illustrated the underlying molecular mechanisms regulated by TET1 in glioma.

Identification and the immunological role of two Nimrod family genes in the silkworm, Bombyx mori.

In animals, immune signaling pathways and effector molecules participate in attenuating microbial infection. Recent work has shown that the Nimrod family proteins can directly bind to bacteria, and this binding leads to bacterial phagocytosis. Although the Nimrod gene family has been reported in many non-drosophilids, their functions remain unexplored in most insect species. Here, we report two members (Nimrod-B and Draper) of the Nimrod gene family from Bombyx mori and analyzed their role in immunity. The two genes were ubiquitously expressed in the tested tissues; but, they transcribed preferentially in immune tissues. The developmental profiles showed that BmNimrod-B and BmDraper transcription levels were highest in the pupal stages. Challenge with microbial pathogens induced the transcription levels of all two genes at different time points. Knockdown of BmDraper decreased the bacterial clearance and increased their replication relative to the control group, whereas, BmNimrod-B suppression had a non-significant effect on them. Furthermore, the mortality rate was increased after BmDraper silencing. The knockdown of these genes did not significantly affect the production of antimicrobial peptides following E. coli infection. Taken together, the Nimrod family genes play a crucial role in host defense by positively regulating the antibacterial immune response in silkworm B. mori.

Long Non-Coding RNA UBA6-AS1 Promotes the Malignant Properties of Glioblastoma by Competitively Binding to microRNA-760 and Enhancing Homeobox A2 Expression.

BACKGROUND: The dysregulation of long non-coding RNAs is a frequent finding in glioblastoma (GBM) and is considered as a crucial mechanism contributing to GBM oncogenesis and progression. The biological roles and underlying mechanisms of action of UBA6 antisense RNA 1 (UBA6-AS1) in GBM have been rarely investigated. Therefore, the aim of the present study was to investigate in detail the role of UBA6-AS1 in the modulation of the malignant properties of GBM and explore the possible underlying mechanism(s). METHODS: The expression of UBA6-AS1 in GBM was determined via reverse transcription-quantitative PCR. Cell Counting Kit-8 assay, flow cytometric analysis, Transwell migration and invasion assays, and in vivo tumorigenicity assay were applied to elucidate the biological effects of UBA6-AS1 on GBM cells. The possible biological events associated with UBA6-AS1 were investigated by luciferase reporter, RNA immunoprecipitation (RIP) and rescue assays. RESULTS: UBA6-AS1 was overexpressed in GBM, which was consistent with the data from The Cancer Genome Atlas database. In the case of UBA6-AS1 depletion, GBM cell proliferation, migration and invasion were notably decreased and cell apoptosis was enhanced in vitro. Additionally, knockdown of UBA6-AS1 suppressed the proliferation of GBM cells in vivo. Mechanistically, UBA6-AS1 functioned as a competing endogenous RNA by adsorbing miR-760 and, consequently, upregulating homeobox A2 (HOXA2) expression. Rescue experiments demonstrated that the UBA6-AS1 silencing-mediated regulatory effects on GBM cells were reversed by the decrease of miR-760 or restoration of HOXA2 expression. CONCLUSION: Therefore, the results of the present study revealed that UBA6-AS1 promoted the malignant progression of GBM via targeting the miR-760/HOXA2 axis, thereby representing a promising effective target for the treatment of GBM.