Dataset Information

Circ_0032821 Facilitates Gastric Cancer Cell Proliferation, Migration, Invasion and Glycolysis by Regulating MiR-1236-3p/HMGB1 Axis.

ABSTRACT: Background:Circular RNAs (circRNAs) play an essential role in the pathogenesis of malignant tumors, including gastric cancer (GC). However, the effect of circ_0032821 on GC remains largely unknown. Methods:QRT-PCR assay was employed to examine the levels of circ_0032821, CEP128 mRNA and miR-1236-3p. RNase R digestion assay was utilized to verify the feature of circ_0032821. Cell Counting Kit-8 (CCK-8) assay and transwell assay were adopted to evaluate cell proliferation and metastasis. The level of glycolysis was evaluated through detecting ECAR, OCR, lactate production, glucose uptake and ATP synthesis. Dual-luciferase reporter assay and RIP assay were conducted to analyze the relationship between miR-1236-3p and circ_0032821 or HMGB1. Western blot assay was adopted for high mobility group box 1 (HMGB1) level. Murine xenograft model assay was utilized for the effect of circ_0032821 in vivo. Results:High level of circ_0032821 was observed in GC tissues and cells. Silencing of circ_0032821 markedly repressed cell proliferation, metastasis and glycolysis in GC cells in vitro and blocked tumorigenesis of GC in vivo. For mechanism analysis, circ_0032821 was identified as the sponge of miR-1236-3p and HMGB1 was the target gene of miR-1236-3p. Moreover, miR-1236-3p suppression restored the influences of circ_0032821 deficiency on GC cell proliferation, metastasis and glycolysis. Overexpression of miR-1236-3p relieved the malignant behaviors of GC cells by targeting HMGB1. Conclusion:Circ_0032821 accelerated GC development through elevating HMGB1 expression via sponging miR-1236-3p.

SUBMITTER: Chen L

PROVIDER: S-EPMC7567569 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Circ_0032821 Facilitates Gastric Cancer Cell Proliferation, Migration, Invasion and Glycolysis by Regulating MiR-1236-3p/HMGB1 Axis.

Chen Lei L Chi Kun K Xiang Huaguo H Yang Yan Y

Cancer management and research 20201012

<h4>Background</h4>Circular RNAs (circRNAs) play an essential role in the pathogenesis of malignant tumors, including gastric cancer (GC). However, the effect of circ_0032821 on GC remains largely unknown.<h4>Methods</h4>QRT-PCR assay was employed to examine the levels of circ_0032821, CEP128 mRNA and miR-1236-3p. RNase R digestion assay was utilized to verify the feature of circ_0032821. Cell Counting Kit-8 (CCK-8) assay and transwell assay were adopted to evaluate cell proliferation and metast ...[more]

PMID: 33116853

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Project description:Background: Hypoxia is a crucial factor in the progression of various tumors, including gastric cancer (GC). Circular RNAs (circRNAs) are important regulators in GC, and this study focused on researching circC6orf132 in GC progression under hypoxia. Methods: In vitro experiments were performed in GC cells under hypoxia (1% O2). CircC6orf132, microRNA-873-5p (miR-873-5p), and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) levels were examined by real-time polymerase chain reaction (qRT-PCR). Colony formation assay and transwell assay were used for detecting cell proliferation and migration or invasion. Glycolytic metabolism was evaluated using lactate production, glucose uptake, and adenosine triphosphate (ATP) level and extracellular acidification rate (ECAR). Western blotting was performed for determining protein expression. The target interaction was analyzed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. In vivo assay was conducted via mouse xenograft model. Results: The expression of circC6orf132 was significantly high in GC cells under hypoxia. Hypoxia-induced GC proliferation, migration, invasion, and glycolysis were reversed by silencing circC6orf132. CircC6orf132 targeted miR-873-5p; and the inhibition of circC6orf132 knockdown for the effects of hypoxia on GC cells was abrogated by miR-873-5p inhibitor. PRKAA1 was validated as a downstream gene of miR-873-5p, and miR-873-5p functioned as an anticancer molecule in GC cells under hypoxia by downregulating PRKAA1 level. CircC6orf132 could regulate PRKAA1 by sponging miR-873-5p. CircC6orf132/miR-873-5p/PRKAA1 axis could regulate GC progression under the hypoxic condition. CircC6orf132 downregulation reduced tumorigenesis in vivo through affecting the miR-873-5p/PRKAA1 axis. Conclusion: CircC6orf132 has been affirmed to promote proliferation, migration, invasion, and glycolysis in GC under hypoxia, partly by depending on the regulation of miR-873-5p/PRKAA1 axis.

Project description:Congenital hypothyroidism (CH) is an endocrine disease caused by congenital thyroid hormone (TH) deficiency. MicroRNAs (miRNAs or miRs) have been reported to inhibit the progression of congenital hypothyroidism. However, the expression and role of miR-1236-3p in CH remains unclear. To address this, 12 day old Sprague-Dawley rats were divided into five groups: Control; Congenital hypothyroidism (CH), miR-1236-3p inhibitor control (inhibitor control); miR-1236-3p inhibitor (inhibitor); and miR-1236-3p inhibitor + translationally-controlled tumor protein 1 (TPT1)-small interfering (si)RNA (inhibitor + siRNA). Propylthiouracil (50 mg/day) was injected intraperitoneally into pregnant rats to generate pups with CH. The levels of miR-1236-3p and TPT1 were detected via reverse transcription-quantitative PCR and western blot analysis. Bioinformatics analysis was performed to predict the targets of miR-1236-3p, which was confirmed using dual luciferase reporter assay. Flow cytometry and MTT assay were used to measure neuronal cell apoptosis and cell viability, whereas western blotting was applied to detect the expression of Pim-3, p-Bad (Ser112), Bad and Bcl-xL, proteins associated with apoptosis. The results revealed that miR-1236-3p expression was significantly upregulated, whilst TPT1 expression was significantly downregulated in the hippocampus tissues of CH rats compared with the control group. TPT1 was confirmed as a target of miR-1236-3p. MiR-1236-3p inhibitor prevented hippocampal neuron apoptosis induced by CH induction, which was reversed by TPT1-siRNA transfection. In addition, following miR-1236-3p inhibitor transfection, neuronal cell apoptosis significantly reduced compared with the control group, which was accompanied by significantly increased expressions of Pim-3, p-Bad (Ser112) and Bcl-xL expression. These effects were reversed by TPT1-siRNA co-transfection. These results indicated that inhibition of miR-1236-3p expression inhibited neuron apoptosis in vivo and in vitro by targeting TPT1, serving a protective role in CH.

Dataset Information

Circ_0032821 Facilitates Gastric Cancer Cell Proliferation, Migration, Invasion and Glycolysis by Regulating MiR-1236-3p/HMGB1 Axis.

Publications

Circ_0032821 Facilitates Gastric Cancer Cell Proliferation, Migration, Invasion and Glycolysis by Regulating MiR-1236-3p/HMGB1 Axis.

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