长非编码 RNA TUG1 通过增强 ZBTB7C 的表达促进骨肉瘤的恶性发展

IF 4.1 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Xueying An , Wenshu Wu , Pu Wang , Abdurahman Mahmut , Junxia Guo , Jian Dong , Wang Gong , Bin Liu , Lin Yang , Yuze Ma , Xingquan Xu , Jianmei Chen , Wangsen Cao , Qing Jiang
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The miRNA targets were identified by transcriptome sequencing and verified by luciferase reporter and RNA pull-down assays. Several <em>in vivo</em> and <em>in vitro</em> approaches, including CCK8 assay, western blot, qRT-PCR, lentiviral transduction and OS cell xenograft mouse model were established to validate the effects of lncTUG1 regulation of miRNA and the downstream target genes on OS cell growth, apoptosis and progression.</p></div><div><h3>Results</h3><p>We found that lncTUG1 and miR-26a-5p were inversely up or down-regulated in OS cells, and siRNA-mediated lncTUG1 knockdown reversed the miR-26a-5p down-regulation and suppressed proliferation and enhanced apoptosis of OS cells. Further, we identified that an oncoprotein ZBTB7C was also upregulated in OS cells that were subjected to lncTUG1/miR-26a-5p regulation. 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引用次数: 0

摘要

背景长非编码 RNA(lncRNA)的失调是肿瘤发生的一个重要组成部分。方法通过生物信息学分析评估了与骨肉瘤进展相关的lncRNA及其调控的miRNA的表达谱,并通过骨肉瘤细胞的qRT-PCR进行了确认。通过转录组测序确定了miRNA的靶标,并通过荧光素酶报告和RNA下拉实验进行了验证。通过CCK8检测、Western印迹、qRT-PCR、慢病毒转导和OS细胞异种移植小鼠模型等多种体内和体外方法,验证了lncTUG1调控miRNA及其下游靶基因对OS细胞生长、凋亡和进展的影响。结果 我们发现,lncTUG1和miR-26a-5p在OS细胞中呈反向上调或下调,siRNA介导的lncTUG1敲除逆转了miR-26a-5p的下调,抑制了OS细胞的增殖并增强了其凋亡。此外,我们还发现,在受到lncTUG1/miR-26a-5p调控的OS细胞中,一种肿瘤蛋白ZBTB7C也出现了上调。结论我们的数据表明,lncTUG1作为miR-26a-5p海绵,通过上调ZBTB7C促进OS进展,靶向lncTUG1可能是治疗OS的有效策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Long noncoding RNA TUG1 promotes malignant progression of osteosarcoma by enhancing ZBTB7C expression

Long noncoding RNA TUG1 promotes malignant progression of osteosarcoma by enhancing ZBTB7C expression

Long noncoding RNA TUG1 promotes malignant progression of osteosarcoma by enhancing ZBTB7C expression

Background

Dysregulation of long non-coding RNAs (lncRNAs) is an important component of tumorigenesis. Aberrant expression of lncRNA taurine upregulated gene 1 (lncTUG1) has been reported in various tumors; however, its precise role and key targets critically involved in osteosarcoma (OS) progression remain unclear.

Methods

The expression profiles of lncRNAs and their regulated miRNAs related to OS progression were assessed by bioinformatics analysis and confirmed by qRT-PCR of OS cells. The miRNA targets were identified by transcriptome sequencing and verified by luciferase reporter and RNA pull-down assays. Several in vivo and in vitro approaches, including CCK8 assay, western blot, qRT-PCR, lentiviral transduction and OS cell xenograft mouse model were established to validate the effects of lncTUG1 regulation of miRNA and the downstream target genes on OS cell growth, apoptosis and progression.

Results

We found that lncTUG1 and miR-26a-5p were inversely up or down-regulated in OS cells, and siRNA-mediated lncTUG1 knockdown reversed the miR-26a-5p down-regulation and suppressed proliferation and enhanced apoptosis of OS cells. Further, we identified that an oncoprotein ZBTB7C was also upregulated in OS cells that were subjected to lncTUG1/miR-26a-5p regulation. More importantly, ZBTB7C knockdown reduced the ZBTB7C upregulation and ZBTB7C overexpression diminished the anti-OS effects of lncTUG1 knockdown in the OS xenograft model.

Conclusions

Our data suggest that lncTUG1 acts as a miR-26a-5p sponge and promotes OS progression via up-regulating ZBTB7C, and targeting lncTUG1 might be an effective strategy to treat OS.

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来源期刊
Biomedical Journal
Biomedical Journal Medicine-General Medicine
CiteScore
11.60
自引率
1.80%
发文量
128
审稿时长
42 days
期刊介绍: Biomedical Journal publishes 6 peer-reviewed issues per year in all fields of clinical and biomedical sciences for an internationally diverse authorship. Unlike most open access journals, which are free to readers but not authors, Biomedical Journal does not charge for subscription, submission, processing or publication of manuscripts, nor for color reproduction of photographs. Clinical studies, accounts of clinical trials, biomarker studies, and characterization of human pathogens are within the scope of the journal, as well as basic studies in model species such as Escherichia coli, Caenorhabditis elegans, Drosophila melanogaster, and Mus musculus revealing the function of molecules, cells, and tissues relevant for human health. However, articles on other species can be published if they contribute to our understanding of basic mechanisms of biology. A highly-cited international editorial board assures timely publication of manuscripts. Reviews on recent progress in biomedical sciences are commissioned by the editors.
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