Peripheral Blood Leukocyte Expression of lncRNA MIAT and Its Diagnostic and Prognostic Value in Ischemic Stroke

Zhu, Man; Li, Nandi; Luo, Ping; Wei, Jing; Xue, Wei; Liang, Chunzi; Tu, Jiancheng

doi:10.1016/j.jstrokecerebrovasdis.2017.09.009

Cited by 84 publications

(58 citation statements)

References 40 publications

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“…Previous studies demonstrated that MIAT was highly expressed in cardiomyocytes, and involved in MI ( Qu X. et al, 2017 ), diabetic cardiomyopathy ( Zhou et al, 2017 ), ischemic stroke ( Zhu et al, 2017 ), angiogenesis ( Yan et al, 2015 ; Jiang et al, 2016 ). Recently, MIAT was found to be an oncogenic lncRNA in various cancers.…”

Section: Discussionmentioning

confidence: 99%

Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a

Luo

et al. 2018

Front. Pharmacol.

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Long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) was recently identified as oncogene in several cancers. However, the role of MIAT on acquired resistance in lung cancer and the underlying mechanisms remain unclear. Here, we showed that the expression of MIAT in lung cancer tissues was upregulated compared with adjacent tissues. LncRNA MIAT expression was associated with tumor size, lymph node metastasis, distant metastasis and TNM stage. Univariate analysis and multivariate analysis revealed that the lncRNA MIAT to be an independent factor for predicating the prognosis of lung cancer patients. Low lncRNA MIAT have longer overall survival time and progression-free survival time than patients with high lncRNA MIAT expression. Moreover, the knockdown of MIAT significantly sensitized PC9 and gefitinib-resistant PC9 cells to gefitinib in vitro and in vivo, and increased the expression of miR-34a and inactivated PI3K/Akt signaling. MIAT interacted with miR-34a and epigenetically controlled the miR-34a expression by hyper-methylating its promotor. Taken together, our findings demonstrated that knockdown of MIAT by siRNA enhances lung cancer cells to gefitinib through the PI3K/Akt signaling pathway by epigenetically regulating miR-34a. Thus, MIAT may be a useful prognostic marker and therapeutic target for lung cancer patients.

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Section: Discussionmentioning

confidence: 99%

Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a

Luo

et al. 2018

Front. Pharmacol.

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“…long non-coding rnas (lncrnas), are non-coding rnas of >200 nucleotides in length that serve important roles in various diseases, such as coronary artery disease, diabetes and cancer (5), and thus, they may represent potential biomarkers for the diagnosis and treatment of aiS. This hypothesis has been validated by numerous previous studies; for example, Zhu et al (6) identified that the expression levels of the lncrna, myocardial infarction-associated transcript (MiaT), were significantly upregulated in blood samples compared with control samples, in addition to demonstrating that MiaT may serve as a potential diagnostic and prognostic indicator for patients with aiS [area under the curve (auc), 0.842; sensitivity, 74.1%; specificity, 80.4%] and prognostic (AUC, 0.791; sensitivity, 79.2%; specificity, 72.9%). Feng et al (7) reported that plasma expression levels of the lncrna, antisense non-coding rna in the inK4 locus (anril), were lower in patients with aiS compared with control samples, with a prediction value for aiS risk of 0.759, and that anril expression also negatively correlated with the national institutes of Health Stroke Scale (niHSS) score.…”

Section: Introductionmentioning

confidence: 81%

Competing endogenous RNA network analysis for screening inflammation‑related long non‑coding RNAs for acute ischemic stroke

et al. 2020

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long non-coding rnas (lncrnas) represent potential biomarkers for the diagnosis and treatment of various diseases; however, the role of circulating acute ischemic stroke (aiS)-related lncrnas remains relatively unknown. The present study aimed to screen crucial lncrnas for aiS based on the competing endogenous rna (cerna) hypothesis. The expression profile datasets for one mrna, accession no. GSe16561, and four micrornas (mirnas), accession nos. GSe95204, GSe86291, GSe55937 and GSe110993, were downloaded from the Gene expression omnibus database. differentially expressed genes (deGs), lncrnas (dels), and mirnas (deMs) were identified, and clusterProfiler was used to interpret the function of the deGs. Based on the protein-protein interaction (PPi) network and module analyses, hub DEGs were identified. A ceRNA network was established based on mirna-mrna or mirna-lncrna interaction pairs. In total, 2,041 DEGs and 5 DELs were identified between the aiS and controls samples in GSe16561, and 10 deMs between at least two of the four miRNA expression profiles. A PPI network was constructed with 1,235 deGs, among which 20 genes were suggested to be hub genes. The hub genes paxillin (PXn), FYn-proto-oncogene, Src family tyrosine kinase (FYn), ras homolog family member a (rHoa), STaT1, and growth factor receptor-bound protein 2 (GrB2), were amongst the most significantly enriched modules extracted from the PPi network. Functional analysis revealed that these hub genes were associated with inflammation-related signaling pathways. an aiS-related cerna network was constructed, in which 4 dels were predicted to function as cernas for 9 deMs, to regulate the five identified hub genes; that is, minichromosome maintenance complex component 3 associated protein-antisense rna 1 (McM3aP-aS1)/long intergenic non-protein coding rna 1089 (linc01089)/hsa-mirna (mir)-125a/FYn, inositol-tetrakisphosphate 1-kinase-antisense rna 1 (iTPK1-aS1)/hsa-let-7i/rHoa/GrB2/STaT1, and human leukocyte antigen complex group 27 (HcG27)/hsamir-19a/PXn interaction axes. in conclusion, McM3aP-aS1, linc01089, iTPK1-aS1, and HcG27 may represent new biomarkers and underlying targets for the treatment of aiS.

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“…Increased levels of lncRNAs H19 and LIPCAR were found in plasma and serum samples in a Chinese population with atherosclerotic disease [83,84]. Further, lncRNA MIAT were detected to be elevated in the blood of ischemic stroke patients [85]. LncRNA SMILR seems to play a role in plaque stability [58], and its plasma levels positively correlate with C-reactive protein [59].…”

Section: Lncrnas As Biomarkers In Atherosclerosismentioning

confidence: 99%

The Long Non-coding Road to Atherosclerosis

Josefs

Boon

2020

Curr Atheroscler Rep

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Purpose of Review To summarize recent insights into long non-coding RNAs (lncRNAs) involved in atherosclerosis. Because atherosclerosis is the main underlying pathology of cardiovascular diseases (CVD), the world's deadliest disease, finding novel therapeutic strategies is of high interest. Recent Findings LncRNAs can bind to proteins, DNA, and RNA regulating disease initiation and plaque growth as well as plaque stability in different cell types such as endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and macrophages. A number of lncRNAs have been implicated in cholesterol homeostasis and foam cell formation such as LASER, LeXis, and CHROME. Among others, MANTIS, lncRNA-CCL2, and MALAT1 were shown to be involved in vascular inflammation. Further regulations include, but are not limited to, DNA damage response in ECs, phenotypic switch of VSMCs, and various cell death mechanisms. Interestingly, some lncRNAs are closely correlated with response to statin treatment, such as NEXN-AS1 or LASER. Additionally, some lncRNAs may serve as CVD biomarkers. Summary LncRNAs are a potential novel therapeutic target to treat CVD, but research of lncRNA in atherosclerosis is still in its infancy. With increasing knowledge of the complex and diverse regulations of lncRNAs in the heterogeneous environment of atherosclerotic plaques, lncRNAs hold promise for their clinical translation in the near future.

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Peripheral Blood Leukocyte Expression of lncRNA MIAT and Its Diagnostic and Prognostic Value in Ischemic Stroke

Cited by 84 publications

References 40 publications

Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a

Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a

Competing endogenous RNA network analysis for screening inflammation‑related long non‑coding RNAs for acute ischemic stroke

The Long Non-coding Road to Atherosclerosis

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