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微小 RNA-1288 通过抑制泛素羧基末端水解酶 CYLD 的表达促进人脑胶质瘤细胞的增殖。

MicroRNA‑1288 promotes cell proliferation of human glioblastoma cells by repressing ubiquitin carboxyl‑terminal hydrolase CYLD expression.

机构信息

Department of Radiation Oncology, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan 610041, P.R. China.

Department of Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.

出版信息

Mol Med Rep. 2017 Nov;16(5):6764-6770. doi: 10.3892/mmr.2017.7481. Epub 2017 Sep 13.

Abstract

Previous studies have demonstrated that microRNAs (miRs) are important regulators involved in various cancers, including human glioblastoma (GBM). However, the underlying mechanism of miR‑1288 remains poorly understood, and its role in GBM has not been reported. The present study confirmed that miR‑1288 expression was markedly upregulated in GBM. Ectopic expression of miR‑1288 promoted the prolife-ration, colony formation and anchorage‑independent growth of GBM cells. Bioinformatics analysis coupled with western blotting and luciferase report assays also indicated that miR‑1288 promoted cell proliferation of GBM by targeting ubiquitin carboxyl‑terminal hydrolase (CYLD). Knockdown of CYLD expression reversed the cell proliferation promotion by miR‑1288‑in in GBM. These results suggest that the miR‑1288/CYLD axis may represent a potential therapeutic target for the treatment of GBM.

摘要

先前的研究表明,微小 RNA(miRs)是参与包括人类脑胶质瘤(GBM)在内的多种癌症的重要调控因子。然而,miR-1288 的潜在机制仍知之甚少,其在 GBM 中的作用尚未见报道。本研究证实 miR-1288 在 GBM 中表达明显上调。miR-1288 的异位表达促进了 GBM 细胞的增殖、集落形成和非锚定依赖性生长。生物信息学分析结合 Western blot 和荧光素酶报告分析也表明,miR-1288 通过靶向泛素羧基末端水解酶(CYLD)促进 GBM 细胞的增殖。GBM 中 CYLD 表达的下调逆转了 miR-1288 诱导的细胞增殖促进作用。这些结果表明,miR-1288/CYLD 轴可能代表治疗 GBM 的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3df/5865833/31e7e98a2abc/mmr-16-05-6764-g00.jpg

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