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Long non-coding RNA MIAT in development and disease: a new player in an old game.

ABSTRACT: Long non-coding RNAs (lncRNAs), which are a portion of non-protein-coding RNAs (ncRNAs), have manifested a paramount role in the pathophysiology of human diseases, particularly in pathogenesis and progression of disease. Myocardial infarction associated transcript (MIAT), which was recently found to demonstrate aberrant expression in various diseases, such as myocardial infarction, schizophrenia, ischemic stroke, diabetic complications, age-related cataract and cancers, is a novel disease-related lncRNA. This work summarize current evidence regarding the biological functions and underlying mechanisms of lncRNA MIAT during disease development.LncRNA MIAT likely represents a feasible cancer biomarker or therapeutic target.

SUBMITTER: Sun C

PROVIDER: S-EPMC5851271 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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Long non-coding RNA MIAT in development and disease: a new player in an old game.

Sun Cheng C Huang Lining L Li Zhenglong Z Leng Kaiming K Xu Yi Y Jiang Xingming X Cui Yunfu Y

Journal of biomedical science 20180313 1

<h4>Background</h4>Long non-coding RNAs (lncRNAs), which are a portion of non-protein-coding RNAs (ncRNAs), have manifested a paramount role in the pathophysiology of human diseases, particularly in pathogenesis and progression of disease. Myocardial infarction associated transcript (MIAT), which was recently found to demonstrate aberrant expression in various diseases, such as myocardial infarction, schizophrenia, ischemic stroke, diabetic complications, age-related cataract and cancers, is a n ...[more]

PMID: 29534728

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Project description:Blood-tumor barrier (BTB) presents a major obstacle to brain drug delivery. Therefore, it is urgent to enhance BTB permeability for the treatment of glioma. In this study, we demonstrated that MIAT, ZAK, and phosphorylated NFκB-p65 (p-NFκB-p65) were upregulated, while miR-140-3p was downregulated in glioma-exposed endothelial cells (GECs) of BTB compared with those in endothelial cells cocultured with astrocytes (ECs) of blood-brain barrier (BBB). MIAT inhibited miR-140-3p expression, increased the expression of ZAK, enhanced the ratio of p-NFκB-p65:NFκB-p65, and promoted the endothelial leakage of BTB. Our current study revealed that miR-140-3p was complementary to the ZAK 3'untranslated regions (3'-UTR), and luciferase activity of ZAK was inhibited by miR-140-3p in 293T cells. MiR-140-3p silencing resulted in an increase in BTB permeability by targeting ZAK, while overexpression of miR-140-3p had the opposite results in GECs of BTB. Overexpression of ZAK induced an increase in BTB permeability, and this effect was related to ZAK's ability to mediate phosphorylation of NFκB-p65. Conversely, ZAK silencing get opposite results in GECs of BTB. As a molecular sponge of miR-140-3p, MIAT attenuated its negative regulation of the target gene ZAK by adsorbing miR-140-3p. P-NFκB-p65 as a transcription factor negatively regulated the expression of TJ-associated proteins by means of chip assay and luciferase assay. Single or combined application of MIAT and miR-140-3p effectively promoted antitumor drug doxorubicin (Dox) across BTB to induce apoptosis of glioma cells. In summary, MIAT functioned as a miR-140-3p sponge to regulate the expression of its target gene ZAK, which contribution to phosphorylation of NFκB-p65 was associated with an increase in BTB permeability by down-regulating the expression of TJ associated proteins, thereby promoting Dox delivery across BTB. These results might provide a novel strategy and target for chemotherapy of glioma.

Project description:Background: Although the treatment of cancer has made evident progress, its morbidity and mortality are still high. A tumor marker is a critical indicator for early cancer diagnosis, and timely cancer detection can efficiently help improve the prognosis of patients. Therefore, it is necessary to identify novel markers associated with cancer. LncRNA myocardial infarction associated transcript (MIAT) is a newly identified tumor marker, and in this study, we aimed to explore the relationship between MIAT and clinicopathological features and patient prognosis. Methods: We searched PubMed, Embase, Web of Science, and The Cochrane Library from inception to September 2020 to identify correlational studies. Then, we extracted valid data and used Stata software to make forest plots. We used the hazard ratio (HR) or odds ratio (OR) with 95% CI to evaluate the relationship between aberrant expression of MIAT and patients' prognosis and clinicopathological features. Results: The study included 21 studies, containing 2,048 patients. Meta-analysis showed that overexpression of lncRNA MIAT was associated with poor overall survival (OS) (HR = 1.60, 95% CI, 1.31-1.96, p < 0.001). In addition, high expression of MIAT could forecast tumor size (OR = 2.26, 95% CI 1.34-3.81, p = 0.002), distant metastasis (OR = 2.54, 95% CI 1.84-3.50, p < 0.001), TNM stage (OR = 2.38, 95% CI 1.36-4.18, p = 0.002), lymph node metastasis (OR = 2.59, 95% CI 1.25-5.36, p = 0.011), and the degree of differentiation (OR = 2.65, 95% CI 1.54-4.58, p < 0.001). However, other clinicopathological features, including age (OR = 1.07, 95% CI 0.87-1.32, p = 0.516), gender (OR = 0.95, 95% CI 0.77-1.19, p = 0.668), and histology (OR = 0.72, 95% CI 0.48-1.10, p = 0.128) were not significantly different from high expression of MIAT. Conclusions: Our study showed that overexpression of MIAT is related to poor overall survival and clinicopathological features. MIAT can be considered a novel tumor marker to help diagnose tumors earlier and improve patient prognosis.

Dataset Information

Long non-coding RNA MIAT in development and disease: a new player in an old game.

Publications

Long non-coding RNA MIAT in development and disease: a new player in an old game.

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