Circ_0016347通过miR-661/IL6R轴调节骨肉瘤细胞的增殖、迁移、侵袭、细胞周期和凋亡。

IF 3.3 4区 医学 Q3 IMMUNOLOGY
Autoimmunity Pub Date : 2022-06-01 Epub Date: 2022-02-15 DOI:10.1080/08916934.2022.2037129
Yan Liu, Jianjun Yuan, Quan Zhang, Zhishuai Ren, Guang Li, Rong Tian
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引用次数: 2

摘要

背景:骨肉瘤是儿童和青少年常见的原发性骨肿瘤。环状rna (circRNAs)在包括骨肉瘤在内的人类疾病中发挥重要作用。因此,我们探索circ_0016347在骨肉瘤中的作用。方法:采用实时定量聚合酶链反应(RT-qPCR)检测circ_0016347、microRNA-661 (miR-661)、白细胞介素-6受体(IL6R)在骨肉瘤组织和细胞中的表达水平。采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基- 2h -四唑-3-溴化铵(MTT)和EdU实验评估骨肉瘤细胞的增殖情况。用transwell法测定其迁移和侵袭。流式细胞术检测细胞周期分布及凋亡情况。通过双荧光素酶报告基因检测分析circ_0016347、miR-661和IL6R之间的关联关系。western blot法检测蛋白表达。为了阐明circ_0016347抑制在体内的功能作用,我们建立了异种移植实验。结果:与对照组相比,Circ_0016347在骨肉瘤组织和细胞中明显过表达。circ_0016347的抑制抑制了骨肉瘤细胞的增殖、迁移、侵袭和细胞周期,并诱导了细胞凋亡,这一过程被miR-661的敲低所推翻。在体内,circ_0016347敲低一致地抑制肿瘤生长。此外,miR-661直接靶向并抑制IL6R, IL6R的上调逆转了miR-661诱导的骨肉瘤细胞效应。此外,circ_0016347可以通过miR-661调控IL6R的表达。circ_0016347的抑制也通过IL6R使骨肉瘤细胞中的Janus kinase 2 (JAK2)/Transcription 3 (STAT3)信号通路失活。结论:Circ_0016347在骨肉瘤中至少部分通过miR-661/IL6R轴和JAK2/STAT3信号通路发挥癌基因的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Circ_0016347 modulates proliferation, migration, invasion, cell cycle, and apoptosis of osteosarcoma cells via the miR-661/IL6R axis.

Background: Osteosarcoma is a common primary bone tumour in children and adolescents. Circular RNAs (circRNAs) exert vital functions in human diseases, including osteosarcoma. Therefore, we explored the role of circ_0016347 in osteosarcoma.

Methods: The real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of circ_0016347, microRNA-661 (miR-661), and Interleukin-6 receptor (IL6R) in osteosarcoma tissues and cells. The proliferation of osteosarcoma cells was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and EdU experiments. The migration and invasion were determined by transwell assay. The cell cycle distribution and apoptosis were assessed by flow cytometry assay. The association relationships among circ_0016347, miR-661, and IL6R were analyzed by dual-luciferase reporter assays. The western blot assay was employed to assay the protein expression. A xenograft experiment was established to clarify the functional role of circ_0016347 inhibition in vivo.

Results: Circ_0016347 was obviously overexpressed in osteosarcoma tissues and cells compared with control groups. The suppression of circ_0016347 impeded proliferation, migration, invasion, and cell cycle and induced apoptosis in osteosarcoma cells, which was overturned by knockdown of miR-661. Consistently, circ_0016347 knockdown repressed tumour growth in vivo. Moreover, miR-661 directly targeted and inhibited IL6R, and the upregulation of IL6R reversed miR-661-induced effects on osteosarcoma cells. Furthermore, circ_0016347 could regulate IL6R expression through miR-661. Inhibition of circ_0016347 also inactivated the Janus kinase 2 (JAK2)/Transcription 3 (STAT3) signalling pathway in osteosarcoma cells by IL6R.

Conclusion: Circ_0016347 functioned as an oncogene in osteosarcoma at least in part by the miR-661/IL6R axis and JAK2/STAT3 signalling pathway.

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来源期刊
Autoimmunity
Autoimmunity 医学-免疫学
CiteScore
5.70
自引率
8.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Autoimmunity is an international, peer reviewed journal that publishes articles on cell and molecular immunology, immunogenetics, molecular biology and autoimmunity. Current understanding of immunity and autoimmunity is being furthered by the progress in new molecular sciences that has recently been little short of spectacular. In addition to the basic elements and mechanisms of the immune system, Autoimmunity is interested in the cellular and molecular processes associated with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, type I diabetes, multiple sclerosis and other systemic and organ-specific autoimmune disorders. The journal reflects the immunology areas where scientific progress is most rapid. It is a valuable tool to basic and translational researchers in cell biology, genetics and molecular biology of immunity and autoimmunity.
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