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Circular RNA ZNF609 enhances proliferation and glycolysis during glioma progression by miR-378b/SLC2A1 axis.

ABSTRACT: Glioma is a prevalent brain malignancy with aggressive progression and with grave prognosis in adults. Circular RNAs have been reported to regulate glioma development and function as the diagnostic, prognostic, and therapeutic biomarkers. In this study, we were interested the function of circular RNA ZNF609 in modulating glioma. Remarkably, knockdown of ZNF609 by siRNA in glioma cells reduced cell viabilities and Edu-positive. The silencing of ZNF609 stimulated the apoptosis of glioma cells. Meanwhile, the ZNF609 depletion inhibited the invasion and migration of glioma cells. In glioma cells, the mRNA and protein expression of E-cadherin was enhanced, while Vimentin was reduced by the inhibition of ZNF609. The glucose uptake, lactate product, and ATP production in glioma cells were suppressed by ZNF609 knockdown. Mechanically, miR-378b was sponged by ZNF609 and targeted SLC2A1 in glioma cells. ZNF609 enhanced SLC2A1 expression by inhibiting miR-378b. The inhibition of miR-378b or the enhancement of SLC2A1 reversed ZNF609 depletion-regulated glioma cell proliferation in vitro. The depletion of ZNF609 suppressed glioma cell growth in the nude mice. Therefore, we concluded that ZNF609 contributed to cell survival and glycolysis of glioma by targeting miR-378b/SLC2A1 axis. ZNF609 and miR-378b may function as potential treatment targets in glioma.

SUBMITTER: Zhao Z

PROVIDER: S-EPMC8457557 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Circular RNA ZNF609 promotes the malignant progression of glioma by regulating miR-1224-3p/PLK1 signaling.

Project description:Objective: Previous studies have demonstrated that circular RNAs (circRNAs) play vital roles in pathological process of various diseases, including tumors. This study aimed at exploring the role and mechanism of circRNA RNA ZNF609 (circ-ZNF609) in the occurrence and development of glioma. Materials and methods: Real-time quantitative PCR (qRT-PCR) was applied to measure the expression of circ-ZNF609, miRNA-1224-3p (miR-1224-3p) and Polo-like kinase 1 (PLK1) in glioma tissues and cell lines. Furthermore, the association between circ-ZNF609 and clinical features of glioma was analyzed. CCK8 assay, EdU assay and Transwell assay were conducted to detect the effect of circ-ZNF609, miR-1224-3p and PLK1 on proliferation, migration and invasion in glioma cells. Then, we investigated the underlying mechanism of circ-ZNF609 by bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation (RIP), qRT-PCR and western blotting assay. Results: Circ-ZNF609 was confirmed prominently upregulated in glioma. Inhibition of circ-ZNF609 could obviously suppress glioma cell proliferation, migration and invasion, while overexpression of circ-ZNF609 promoted glioma growth and metastasis. In vivo, xenotransplanted tumor model also showed that overexpression of circ-ZNF609 could promote in vivo glioma growth. Mechanistically, circ-ZNF609 could promote PLK1 expression via binding to miR-1224-3p, circ-ZNF609/miR-1224-3p/PLK1 was shown responsible for circ-ZNF609 promoting glioma growth and metastasis. Conclusion: Together, our results revealed that circ-ZNF609 elevates glioma growth and metastasis via enforcing PLK1 expression by competitively binding miR-1224-3p, suggesting that circ-ZNF609 might be an underlying therapeutic target for glioma.

| S-EPMC8100806 | biostudies-literature

Circular RNA circitga7 accelerates glioma progression via miR-34a-5p/VEGFA axis.

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| S-EPMC8148479 | biostudies-literature

Circular RNA ZNF609 Promoted Hepatocellular Carcinoma Progression by Upregulating PAP2C Expression via Sponging miR-342-3p.

Project description:Background:Emerging evidence has revealed that circular RNAs (circRNAs) participated in hepatocellular carcinoma (HCC) development. However, the roles of most circRNAs have not been studied. Methods:CircZNF609, miR-342-3p and RAP2C expressions were assessed by qPCR or Western blot. Loss-of-function experiments were performed using si-circZNF609 transfection, followed by CCK-8 assay, flow cytometry, wound healing assay and transwell assay. Informatic tools and rescue experiments were carried out to investigate the underlying mechanisms. Results:We showed that circZNF609 was overexpressed in HCC tissues and cells, as well as associated with poor clinical characteristics. Depletion of circZNF609 restrained HCC cell viability, migration and invasion while enhanced cell apoptosis. As to mechanism, miR-342-3p was sponged by circZNF609, and RAP2C was targeted by miR-342-3p. The effects on HCC cells induced by si-circZNF609 could be reversed by miR-342-3p inhibitor or RAP2C. In vivo, circZNF609 knockdown inhibited tumorigenesis of HCC mice, confirming the findings in vitro. Conclusion:CircZNF609 was highly expressed in HCC tissues and driven HCC progression by sponging miR-342-3p and upregulating RAP2C. This study may provide new potential therapeutic targets for HCC treatment.

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miR-148b inhibits glycolysis in gastric cancer through targeting SLC2A1.

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CircHECTD1 Regulates Cell Proliferation and Migration by the miR-320-5p/SLC2A1 Axis in Glioblastoma Multiform.

Project description:Glioblastoma multiform (GBM) is the most common and malignant primary brain cancer in adults, and thus, novel potential therapeutic targets for diagnosis and treatment are urgently needed. Circular RNAs (circRNAs) are a class of widespread and diverse endogenous RNAs that have been suggested as potential critical mediators during progression of various tumors. In this study, we investigated the involvement of circHECTD1 in GBM progression. CircHECTD1 Lentivirus, miR-320-5p mimic, and SLC2A1 Lentivirus were transduced into cancer cells independently or together. circHECTD1, miR-320-5p, and SLC2A1 level were detected by qRT-PCR. Western blot and qRT-PCR were applied to measure the expression of SLC2A1, CyclinD1, CDK2, and PCNA. Flow cytometry, EdU, colony formation, Transwell and wound-healing assays were conducted to assess cell proliferation and migration. Luciferase reporter assays were performed to determine the effect of miR-320-5p on circHECTD1 or SLC2A1. Xenograft experiments were implemented to evaluate tumor growth in vivo. CircHECTD1 expression led to the promotion of proliferation and migration of GBM cells. In addition, circHECTD1 acted as a ceRNA to interact with miR-320-5p, which targeted the solute carrier family 2 member 1 (SLC2A1). In vivo experiments also revealed that circHECTD1 promoted tumor growth. Collectively, our findings showed that the circHECTD1-miR-320-5p-SLC2A1 regulatory pathway promoted the progression of GBM, suggesting that circHECTD1 may be a therapeutic target for GBM.

| S-EPMC8166227 | biostudies-literature

Circular RNA-ZNF609 regulates retinal neurodegeneration by acting as miR-615 sponge.

Project description:Glaucoma is a major cause of visual impairment characterized by progressive retinal neurodegeneration. Circular RNAs are a class of endogenous noncoding RNAs that regulate gene expression in eukaryotes. In this study, we investigated the role of cZNF609 in retinal neurodegeneration induced by glaucoma. Methods: qRT-PCR and Sanger sequencing were conducted to detect cZNF609 expression pattern during retinal neurodegeneration. Immunofluorescence staining was conducted to detect the effect of cZNF609 silencing on retinal neurodegeneration in vivo. MTT assay, Ki67 staining, and PI staining were conducted to detect the effect of cZNF609 silencing on retinal glial cells and RGC function in vitro. Bioinformatics analysis, RNA pull-down assays, and in vitro studies were conducted to reveal the mechanism of cZNF609-mediated retinal neurodegeneration. Results: cZNF609 expression was significantly up-regulated during retinal neurodegeneration. cZNF609 silencing reduced retinal reactive gliosis and glial cell activation, and facilitated RGC survival in vivo. cZNF609 silencing directly regulated Müller cell function but indirectly regulated RGC function in vitro. cZNF609 acted as an endogenous miR-615 sponge to sequester and inhibit miR-615 activity, which led to increased METRN. METRN overexpression could partially rescue cZNF609 silencing-mediated inhibitory effects on retinal glial cell proliferation. Conclusion: Intervention of cZNF609 expression is a promising therapeutic strategy for retinal neurodegeneration.

| S-EPMC6010990 | biostudies-literature

Circular RNA circRNA_103809 Accelerates Bladder Cancer Progression and Enhances Chemo-Resistance by Activation of miR-516a-5p/FBXL18 Axis.

Project description:Background:Numerous researches have suggested that circular RNAs (circRNAs) play critical functions in bladder cancer (BC) progression. This study aims to investigate the potential roles of circRNA_103809 in regulating BC development. Methods:qRT-PCR was used to analyze gene expression. CCK8 and colony formation were used to analyze cell proliferation. Transwell was utilized to examine cell migration and invasion. Gemcitabine was used to analyze the effect of circRNA_103809 on the chemo-resistance of BC cells. Luciferase reporter assay was performed to detect the RNA interactions. Results:circRNA_103809 was highly expressed in BC tissues and cell lines. CircRNA_103809 high expression was associated with a poor progression in BC patients. CircRNA_103809 knockdown impaired the growth and metastasis of BC cells. Furthermore, circRNA_103809 silencing increased the sensitivity of BC cells to Gemcitabine treatment. CircRNA_103809 was the sponge for miR-516a-5p and promoted FBXL18 expression via restraining miR-516a-5p activity. Conclusion:circRNA_103809 promotes proliferation, migration, invasion and chemo-resistance of BC cells through regulating miR-516a-5p/FBXL18 axis.

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Circular RNA hsa_circ_0005909 modulates osteosarcoma progression via the miR-936/HMGB1 axis.

Project description:BackgroundOsteosarcoma (OS) is the most common bone malignant tumor in children, youth, and adolescents. Circular RNA hsa_circ_0005909 (circ_0005909) is involved in the progression of OS. Nevertheless, there are few reports on the role and mechanism of circ_0005909 in OS.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was executed to examine the expression of circ_0005909, miR-936, and High Mobility Group Box 1 (HMGB1) mRNA in OS tissues and cells. Cell viability, colony formation, migration, and invasion were evaluated by Cell Counting Kit-8 (CCK-8), cell colony formation, or transwell assays. Cell epithelial-mesenchymal transition (EMT) and HMGB1 protein levels were assessed through western blot analysis. The role of circ_0005909 on tumor growth in vivo was verified by xenograft assay. The relationship between circ_0005909 or HMGB1 and miR-936 was confirmed with the dual-luciferase reporter or RNA pull-down assays.ResultsCirc_0005909 level was upregulated in OS tissues and cells. OS patients with high circ_0005909 expression had a lower survival rate. Circ_0005909 inhibition reduced tumor growth in vivo and constrained cell viability, colony formation, migration, invasion, and EMT of OS cells in vitro. Furthermore, circ_0005909 served as a sponge for miR-936 and the repressive impacts of circ_0005909 silencing on malignant behaviors of OS cells were abolished by miR-936 inhibitors. Also, HMGB1 acted as a target for miR-936 and was modulated by circ_0005909 via miR-936. Additionally, HMGB1 overexpression restored the inhibitory influence on the malignant behaviors of OS cells mediated by circ_0005909 inhibition.ConclusionsCirc_0005909 inhibition impeded the progression of OS via downregulating HMGB1 via sponging miR-936.

| S-EPMC7359231 | biostudies-literature

CircNFIX promotes progression of glioma through regulating miR-378e/RPN2 axis.

Project description:BACKGROUND:Circular RNA nuclear factor I X (circNFIX) has been reported to play an important role in glioma progression. However, the mechanism by which circNFIX participates in glioma progression remains poorly understood. METHODS:GERIA online were used to analyze the abnormally expressed genes in glioma tissues. The expression levels of circNFIX, microRNA (miR)-378e and Ribophorin-II (RPN2) were measured by quantitative real-time polymerase chain reaction or western blot. Cell cycle distribution, apoptosis, glycolysis, migration and invasion were determined by flow cytometry, special kit and trans-well assays, respectively. The target association between miR-378e and circNFIX or RPN2 was confirmed by luciferase reporter assay, RNA immunoprecipitation and pull-down. Xenograft model was established to investigate the role of circNFIX in vivo. RESULTS:The expression of circNFIX was enhanced in glioma tissues and cells compared with matched controls and high expression of circNFIX indicated poor outcomes of patients. Knockdown of circNFIX led to arrest of cell cycle, inhibition of glycolysis, migration and invasion and promotion of apoptosis in glioma cells. circNFIX was a sponge of miR-378e. miR-378e overexpression suppressed cell cycle process, glycolysis, migration and invasion but promoted apoptosis. miR-378e silence abated the suppressive role of circNFIX knockdown in glioma progression. RPN2 as a target of miR-378e was positively regulated via circNFIX by competitively sponging miR-378e. Silencing circNFIX decreased glioma xenograft tumor growth by regulating miR-378e/RPN2 axis. CONCLUSION:Knockdown of circNFIX inhibits progression of glioma in vitro and in vivo by increasing miR-378e and decreasing RPN2, providing a novel mechanism for understanding the pathogenesis of glioma.

| S-EPMC6936104 | biostudies-literature

Circular RNA circSCAF11 Accelerates the Glioma Tumorigenesis through the miR-421/SP1/VEGFA Axis.

Project description:Circular RNAs (circRNAs) are a novel category of non-coding RNAs, and they have been identified to participate in glioma tumorigenesis. Here we investigated the functions of circRNA circSCAF11 in glioma genesis, and we unveiled its molecular mechanism in the pathophysiological process. Expression levels of circSCAF11, miR-421, and SP1 mRNA were measured using RT-PCR. Proteins were measured using western blotting. The tumor phenotypes of glioma cells were detected using flow cytometry and Cell Counting Kit-8 (CCK-8), transwell, and xenograft mouse assays. The combination within circSCAF11, miR-421, and SP1 was validated using luciferase reporter assay or RNA pull-down assay. The binding of transcription factor SP1 with vascular endothelial cell growth factor A (VEGFA) promoter was inspected using chromatin immunoprecipitation (ChIP). circSCAF11 expression was found to be significantly upregulated in the glioma tissue specimens and cell lines. The ectopic overexpression of circSCAF11 was closely correlated with the poor clinical outcome of glioma patients. Functionally, knockdown of circSCAF11 inhibited the proliferation, invasion, and tumor growth and induced the G0/G1 phase arrest. Mechanically, circSCAF11 positively regulated the SP1 expression through sponging miR-421. Moreover, transcription factor SP1 activated the transcription of VEGFA, constructing the circSCAF11/miR-421/SP1/VEGFA axis in the glioma genesis. The findings in this research illustrate that circSCAF11 accelerates glioma tumorigenesis through the miR-421/SP1/VEGFA axis, providing a potential target for circRNA and glioma treatment.

| S-EPMC6700438 | biostudies-literature

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