Deciphering the role of non-coding RNAs SNHG18, HOXA11-AS, MEG3, and MDC1-AS1 in glioma patients: A combined experimental and computational study

IF 1 Q4 GENETICS & HEREDITY Gene Reports Pub Date : 2024-07-14 DOI:10.1016/j.genrep.2024.101973

Kamal Mohammadian , Arash Moradi , Mansoureh Shabani , Somayeh Kazemi , Shahla Mohammad Ganji

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Abstract

Background

Gliomas are brain tumours categorised into low-grade (I and II) and high-grade (III and IV). Unfortunately, patients with high-grade gliomas have a poor prognosis, which is why researchers are working to improve their management. One crucial area of study is the understanding of glioma tumorigenesis and progression. Recent research has shown that long non-coding RNAs (lncRNAs) play a potential role in this process.

Material and methods

We evaluated the expression of SNHG18, HOXA11-AS, MEG3, and MDC1-AS1 in 150 paraffin tissue block samples, including 37 low-grade gliomas, 58 high-grade gliomas, and 55 non-tumoural tissues. After RNA extraction and complementary DNA synthesis (cDNA), we used probe-based qPCR to evaluate the lncRNA expression level, followed by statistical analyses.

Results

The qRT-PCR analysis revealed differential expression patterns of lncRNAs in tumour tissues compared to controls. In low-grade tumours, SNHG18 and HOXA11-AS were upregulated (SNHG18: 1.78 ± 0.21, p < 0.001; HOXA11-AS: 1.24 ± 0.60, p < 0.001), while MEG3 and MDC1-AS1 were downregulated (MEG3: 0.72 ± 0.17, p < 0.001; MDC1-AS1: 0.24 ± 0.18, p < 0.001). In high-grade tumours, SNHG18 and HOXA11-AS were further upregulated (SNHG18: 3.16 ± 0.88, p < 0.001; HOXA11-AS: 3.83 ± 0.82, p < 0.001), and MEG3 and MDC1-AS1 remained downregulated (MEG3: 0.49 ± 0.29, p < 0.001; MDC1-AS1: 0.15 ± 0.09, p < 0.001). The bioinformatic-based study conveyed that the alteration in lncRNAs expression leads to dysregulation of RNA Polymerase II, which is observed in glioblastoma.

Conclusion

Our results suggest that SNHG18 and HOXA11-AS (up-regulated) may act as oncogenes in high-grade gliomas. In contrast, the downregulation of MEG3 and MDC1-AS1 in high-grade gliomas could be related to tumour suppressor properties. Therefore, it could be assumed that the expression levels of these lncRNAs may serve as potential biomarkers for diagnostic and therapeutic purposes.

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破解非编码 RNA SNHG18、HOXA11-AS、MEG3 和 MDC1-AS1 在胶质瘤患者中的作用：实验与计算相结合的研究

背景胶质瘤是一种脑肿瘤，分为低级别（I 级和 II 级）和高级别（III 级和 IV 级）。不幸的是，高级别胶质瘤患者的预后较差，因此研究人员正在努力改善对他们的治疗。一个重要的研究领域是了解胶质瘤的肿瘤发生和发展。最近的研究表明，长非编码 RNA（lncRNA）在这一过程中发挥着潜在的作用。材料与方法我们评估了 150 份石蜡组织块样本中 SNHG18、HOXA11-AS、MEG3 和 MDC1-AS1 的表达情况，其中包括 37 份低级别胶质瘤样本、58 份高级别胶质瘤样本和 55 份非肿瘤组织样本。结果 qRT-PCR分析显示，与对照组相比，lncRNA在肿瘤组织中的表达模式存在差异。在低级别肿瘤中，SNHG18和HOXA11-AS上调（SNHG18：1.78 ± 0.21，p <；0.001；HOXA11-AS：1.24 ± 0.60，p <；0.001），而MEG3和MDC1-AS1下调（MEG3：0.72 ± 0.17，p <；0.001；MDC1-AS1：0.24 ± 0.18，p <；0.001）。在高级别肿瘤中，SNHG18和HOXA11-AS进一步上调（SNHG18：3.16 ± 0.88，p <；0.001；HOXA11-AS：3.83 ± 0.82，p <；0.001），而MEG3和MDC1-AS1仍然下调（MEG3：0.49 ± 0.29，p <；0.001；MDC1-AS1：0.15 ± 0.09，p <；0.001）。基于生物信息学的研究表明，lncRNAs表达的改变导致了RNA聚合酶II的失调，这在胶质母细胞瘤中是可以观察到的。相反，MEG3 和 MDC1-AS1 在高级别胶质瘤中的下调可能与肿瘤抑制特性有关。因此，可以认为这些lncRNA的表达水平可作为诊断和治疗的潜在生物标志物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Gene Reports Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

3.30

自引率

7.70%

发文量

246

审稿时长

49 days

期刊介绍： Gene Reports publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses. Gene Reports strives to be a very diverse journal and topics in all fields will be considered for publication. Although not limited to the following, some general topics include: DNA Organization, Replication & Evolution -Focus on genomic DNA (chromosomal organization, comparative genomics, DNA replication, DNA repair, mobile DNA, mitochondrial DNA, chloroplast DNA). Expression & Function - Focus on functional RNAs (microRNAs, tRNAs, rRNAs, mRNA splicing, alternative polyadenylation) Regulation - Focus on processes that mediate gene-read out (epigenetics, chromatin, histone code, transcription, translation, protein degradation). Cell Signaling - Focus on mechanisms that control information flow into the nucleus to control gene expression (kinase and phosphatase pathways controlled by extra-cellular ligands, Wnt, Notch, TGFbeta/BMPs, FGFs, IGFs etc.) Profiling of gene expression and genetic variation - Focus on high throughput approaches (e.g., DeepSeq, ChIP-Seq, Affymetrix microarrays, proteomics) that define gene regulatory circuitry, molecular pathways and protein/protein networks. Genetics - Focus on development in model organisms (e.g., mouse, frog, fruit fly, worm), human genetic variation, population genetics, as well as agricultural and veterinary genetics. Molecular Pathology & Regenerative Medicine - Focus on the deregulation of molecular processes in human diseases and mechanisms supporting regeneration of tissues through pluripotent or multipotent stem cells.