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COX10-AS1 Facilitates Cell Proliferation and Inhibits Cell Apoptosis in Glioblastoma Cells at Post-Transcription Level.
Neurochemical Research ( IF 4.4 ) Pub Date : 2020-08-08 , DOI: 10.1007/s11064-020-03081-4
Chaoyang Zhou 1 , Xingxing Jiang 1 , Aijun Liang 1 , Ronglan Zhu 1 , Yu Yang 1 , Liangchen Zhong 1 , Dengfeng Wan 1
Affiliation  

Glioblastoma (GBM) is an invasive cancer with poor prognosis in patients. Researching on molecular functions in GBM has attracted more and more attention. Actin gamma 1 (ACTG1) was reported as a pathogenic gene in skin cancer and colorectal cancer. Present study was designed to explore the biological role and underlying mechanism of ACTG1 in GBM cells. It was uncovered that ACTG1 presented high expression trends in GBM cells. Moreover, ACTG1 suppression hindered cell proliferation and boosted cell apoptosis in GBM. Then, according to the results of bioinformatics analysis and mechanism assays including RIP, RNA pull down and luciferase reporter assay, ACTG1 was verified to be targeted by miR-361-5p in GBM. Next, COX10-AS1 (COX10 antisense RNA 1) was identified as an endogenous sponge for miR-361-5p in GBM. Moreover, COX10-AS1 acted as a competing endogenous RNA (ceRNA) to positively regulate ACTG1 expression via sponging miR-361-5p. The following rescue assays demonstrated that COX10-AS1 promoted GBM cell proliferation and inhibited GBM cell apoptosis through ACTG1 up-regulation at a miR-361-5p dependent way. On the whole, present study uncovered a novel ceRNA pattern in which COX10-AS1 sponged miR-361-5p to elevate ACTG1 expression, therefore accelerating tumorigenesis in GBM. The findings suggested new promising targets for GBM treatment.



中文翻译:

在转录后水平,COX10-AS1促进胶质母细胞瘤细胞的细胞增殖并抑制细胞凋亡。

胶质母细胞瘤(GBM)是一种预后不良的浸润性癌症。GBM中分子功能的研究引起了越来越多的关注。肌动蛋白γ1(ACTG1)被报道为皮肤癌和结肠直肠癌的致病基因。本研究旨在探讨ACTG1在GBM细胞中的生物学作用及其潜在机制。已经发现ACTG1在GBM细胞中呈现高表达趋势。此外,ACTG1抑制抑制GBM中的细胞增殖并促进细胞凋亡。然后,根据生物信息学分析结果和包括RIP,RNA下拉和萤光素酶报告基因检测在内的机理分析,证实ACTG1被GBM中的miR-361-5p靶向。接下来,在GBM中将COX10-AS1(COX10反义RNA 1)鉴定为miR-361-5p的内源海绵。此外,COX10-AS1充当竞争性内源RNA(ceRNA),可通过海绵miR-361-5p积极调节ACTG1的表达。以下救援试验表明,COX10-AS1通过ACTG1上调(以miR-361-5p依赖性)促进GBM细胞增殖并抑制GBM细胞凋亡。总体而言,目前的研究揭示了一种新型的ceRNA模式,其中COX10-AS1用miR-361-5p增强了ACTG1的表达,从而加速了GBM中的肿瘤发生。这些发现为GBM治疗提出了新的有希望的目标。目前的研究发现了一种新的ceRNA模式,其中COX10-AS1敲击miR-361-5p以提高ACTG1表达,从而加速GBM中的肿瘤发生。这些发现为GBM治疗提出了新的有希望的目标。目前的研究发现了一种新的ceRNA模式,其中COX10-AS1敲击miR-361-5p以提高ACTG1表达,从而加速GBM中的肿瘤发生。这些发现为GBM治疗提出了新的有希望的目标。

更新日期:2020-08-09
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