Dataset Information

Circ?TOP2A acts as a ceRNA for miR?346 and contributes to glioma progression via the modulation of sushi domain?containing 2.

ABSTRACT: Dysregulated circular RNAs (circRNAs) are involved in the carcinogenesis and progression of multiple human malignancies. Knowledge of circRNAs in glioma (GM) is limited and further study to uncover new therapeutic targets for GM is urgently required. The present study demonstrated that circ?TOP2A was elevated in GM tissue specimens and cells and that circ?TOP2A levels indicated an unfavorable clinical prognosis in GM. Functionally, circ?TOP2A knockdown reduced viability, migration and invasion and triggered apoptosis in LN229 cells. Ectopic expression of circ?TOP2A aggravated these malignant behaviors in U87MG cells. In terms of mechanism, RNA?seq was performed to discover the potential targets regulated by circ?TOP2A. Circ?TOP2A acted as a competing endogenous RNA to upregulate sushi domain?containing 2 (SUSD2) expression by sponging microRNA (miR) 346. Rescue assays revealed that the oncogenic function of circ?TOP2A was partially dependent on its regulation of the miR?346/SUSD2 axis. In conclusion, the present study identified that circ?TOP2A promoted GM proliferation and aggressiveness via miR?346/SUSD2 signaling, which is a potential prognostic biomarker and therapeutic target for GM.

SUBMITTER: Sang J

PROVIDER: S-EPMC7893696 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature

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Circ‑TOP2A acts as a ceRNA for miR‑346 and contributes to glioma progression via the modulation of sushi domain‑containing 2.

Sang Junzhi J Li Xing X Lv Luting L Zhang Chunyu C Zhang Xiaoqian X Li Guoan G

Molecular medicine reports 20210204 4

Dysregulated circular RNAs (circRNAs) are involved in the carcinogenesis and progression of multiple human malignancies. Knowledge of circRNAs in glioma (GM) is limited and further study to uncover new therapeutic targets for GM is urgently required. The present study demonstrated that circ‑TOP2A was elevated in GM tissue specimens and cells and that circ‑TOP2A levels indicated an unfavorable clinical prognosis in GM. Functionally, circ‑TOP2A knockdown reduced viability, migration and invasion a ...[more]

PMID: 33537815

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Project description:Background: Oxidative stress has emerged as an essential factor in the pathogenesis of intestinal ischemia/reperfusion (I/R) injury. The adaptor protein p66Shc is a key regulator of reactive oxygen species (ROS) generation and a mediator of I/R damage in the intestine, but the upstream mechanisms that directly regulate p66Shc expression during intestinal I/R remain largely unknown. Recent studies have suggested that noncoding RNAs, such as circular RNAs (circRNAs), are important players in physiological and pathological processes based on their versatile regulatory roles in gene expression. The aim of this study was to elucidate the contribution of p66Shc to oxidative damage in intestinal I/R and to investigate the regulation of p66Shc by circRNA sponges. Methods: Intestinal I/R was induced in mice via superior mesenteric artery (SMA) occlusion. A miR-339-5p agomir or circ-protein kinase C beta (PRKCB) siRNA was injected intravenously before I/R challenge. In addition, Caco-2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro to simulate an in vivo I/R model. Results: In vitro, p66Shc deficiency significantly reduced H/R-induced ROS overproduction by attenuating mitochondrial superoxide anion (O2 -) levels, suppressing NADPH oxidase activity and enhancing antioxidant enzyme expression. Moreover, miR-339-5p was identified to directly regulate p66Shc expression in the intestine. Furthermore, we found that a circRNA transcribed from the PRKCB gene, named circ-PRKCB, acted as an endogenous miR-339-5p sponge to regulate p66Shc expression. circ-PRKCB silencing or miR-339-5p overexpression significantly downregulated p66Shc expression and attenuated oxidative stress levels and I/R injury in vivo and in vitro. Notably, the increased circ-PRKCB levels and decreased miR-339-5p levels associated with murine intestinal I/R were consistent with those in patients with intestinal infarction. Conclusions: Our findings reveal a crucial role for the circ-PRKCB/miR-339-5p/p66Shc signaling pathway in regulating oxidative stress in the I/R intestine. This pathway may be a potential therapeutic target for intestinal I/R injury.

Dataset Information

Circ?TOP2A acts as a ceRNA for miR?346 and contributes to glioma progression via the modulation of sushi domain?containing 2.

Publications

Circ‑TOP2A acts as a ceRNA for miR‑346 and contributes to glioma progression via the modulation of sushi domain‑containing 2.

Similar Datasets

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