The role of long non-coding RNA MIAT in cancers

Da, Chao-Ming; Gong, Chang; Wu, Nan; Zhou, Kaisheng; Wu, Zhi-Xi; Zhang, Haihong

doi:10.1016/j.biopha.2020.110359

Cited by 39 publications

(33 citation statements)

References 101 publications

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“…lncRNAs participate in transcriptional modulation, splicing regulation, post-transcriptional process, chromatin remodeling, or protein-protein, protein-DNA, and protein-RNA interactions ( 43 , 44 , 45 ). Myocardial infarction-associated transcript (MIAT) known as retina non-coding RNA2, locates on the human chromosome 12q12.1 ( 31 , 46 ). It has been reported that lncRNA MIAT acts as an oncogene upregulated in various cancers such as gastric cancer, liver cancer, colorectal cancer, and lung cancer ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

“…Myocardial infarction-associated transcript (MIAT) known as retina non-coding RNA2, locates on the human chromosome 12q12.1 ( 31 , 46 ). It has been reported that lncRNA MIAT acts as an oncogene upregulated in various cancers such as gastric cancer, liver cancer, colorectal cancer, and lung cancer ( 31 ). lncRNA MIAT is involved in regulating proliferation, migration, invasion, drug resistance, and cell cycle by targeting some proteins, including MMP9, SF1, TDP43, ZEB1, MYO1B, SGK1, WNT9A, DDX5, and HDAC4 ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that lncRNA MIAT acts as an oncogene upregulated in various cancers such as gastric cancer, liver cancer, colorectal cancer, and lung cancer ( 31 ). lncRNA MIAT is involved in regulating proliferation, migration, invasion, drug resistance, and cell cycle by targeting some proteins, including MMP9, SF1, TDP43, ZEB1, MYO1B, SGK1, WNT9A, DDX5, and HDAC4 ( 31 ). However, the role of lncRNA MIAT in cisplatin-resistant NPC cells is barely known.…”

Section: Discussionmentioning

confidence: 99%

“…Long non-coding RNAs (lncRNAs), known as non-coding singlestrand RNAs, play an essential role as carcinogenic genes or tumor suppressors in the development of human cancer (31)(32)(33)(34). Myocardial infarction-associated transcript (MIAT) was first identified as an lncRNA in 2006 and is considered as a regulator in the nucleus interacting with nuclear factors, while as a competitive endogenous RNA (ceRNA) in the cytoplasm (31,35,36).…”

Section: Introductionmentioning

confidence: 99%

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lncRNA MIAT/HMGB1 Axis Is Involved in Cisplatin Resistance via Regulating IL6-Mediated Activation of the JAK2/STAT3 Pathway in Nasopharyngeal Carcinoma

et al. 2021

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Cisplatin-based chemotherapy and radiotherapy are the main first-line treatment strategies for nasopharyngeal carcinoma (NPC) patients. Unfortunately, resistance is a major obstacle in the clinical management of NPC patients. We prove that the expression level of high-mobility group box 1 (HMGB1) is dramatically increased in resistant NPC cells than that in sensitive cells. HMGB1 induces the expression and secretion of IL6, which leads to constitutive autocrine activation of the JAK2/STAT3 pathway and eventually contributes to chemoresistance in NPC cells. Long non-coding RNAs (lncRNAs) have been identified as key regulators involved in drug resistance. In this study, using GO analysis of the biological process and differential expression analysis, we find 12 significantly altered IncRNAs in NPC cell lines, which may be involved in regulating gene expression. Furthermore, we determine that elevated lncRNA MIAT level upregulates HMGB1 expression, contributing to cisplatin resistance in NPC cells. We find that the deficiency of the lncRNA MIAT/HMGB1 axis, inhibition of JAK2/STAT3, or neutralization of IL6 by antibodies significantly re-sensitizes resistant NPC cells to cisplatin in resistant NPC cells. Moreover, we provide the in vivo evidence that the deficiency of HMGB1 reduces cisplatin-resistant tumor growth. Most importantly, we provide clinical evidence showing that the expression level of the lncRNA MIAT/HMGB1/IL6 axis is elevated in resistant NPC tumors, which is highly correlated with poor clinical outcome. Our findings identify a novel chemoresistance mechanism regulated by the lncRNA MIAT/HMGB1/IL6 axis, which indicates the possibilities for lncRNA MIAT, HMGB1, and IL6 as biomarkers for chemoresistance and targets for developing novel strategies to overcome resistance in NPC patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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lncRNA MIAT/HMGB1 Axis Is Involved in Cisplatin Resistance via Regulating IL6-Mediated Activation of the JAK2/STAT3 Pathway in Nasopharyngeal Carcinoma

et al. 2021

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“…Till now, multiple lines of research have suggested that lncRNAs have critical effects on tumour processes, such as proliferation, apoptosis, and invasion [24][25][26]. COX10-AS1, a lncRNA transcript from chromosome 17, has been shown to be related to the development of human cancers.…”

Section: Discussionmentioning

confidence: 99%

The COX10-AS1/miR-641/E2F6 Feedback Loop Is Involved in the Progression of Glioma

Liu

et al. 2020

SSRN Journal

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Background Glioma is the most common primary tumour of the central nervous system and is considered one of the greatest challenges for neurosurgery. Mounting evidence has shown that lncRNAs participate in various biological processes of tumours, including glioma. This study aimed to reveal the role and relevant mechanism of COX10-AS1 in glioma. Methods The expression of COX10-AS1, miR-641 and E2F6 was measured by qRT-PCR and/or western blot. Clone formation assays, EdU assays, Transwell assays and tumour xenograft experiments were performed to evaluate the effects of COX10-AS1, miR-641 and E2F6 on glioma proliferation, migration and invasion. Luciferase reporter assays, RNA pull-down assays and ChIP assays were conducted to analyse the relationship among COX10-AS1, miR-641 and E2F6. Results First, we demonstrated that COX10-AS1 was upregulated in glioma tissues and cell lines, which was related to the grade of glioma and patient survival. Next, through functional assays, we found that COX10-AS1 in uenced the proliferation, migration and invasion of glioma cell lines. Then, with the help of bioinformatics analysis, we con rmed that COX10-AS1 regulated glioma by acting as a sponge of miR-641 to regulate E2F6. Moreover, further study indicated that E2F6 could promote COX10-AS1 expression by binding to its promoter region. Conclusions COX10-AS1 acts as an oncogene in combination with COX10-AS1/miR-641/E2F6 in glioma, which may be bene cial to the diagnosis and treatment of glioma.

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Serum extracellular vesicles containing MIAT induces atrial fibrosis, inflammation and oxidative stress to promote atrial remodeling and atrial fibrillation via blockade of miR‐485‐5p‐mediated CXCL10 inhibition

Chen

et al. 2021

Clinical & Translational Med

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Background Atrial fibrillation (AF), a supraventricular arrhythmia that impairs cardiac function, is a main source of morbidity and mortality. Serum‐derived extracellular vesicles (EVs) have been identified to carry potential biomarker or target for the diagnosis and treatment of AF. We intended to dissect out the role of lncRNA MIAT enriched in serum‐derived EVs in AF. Methods MIAT expression was quantified in EVs isolated from serum samples of AF patients. Mouse and cell models of AF were developed after angiotensin II (Ang II) induction. Relationship between MIAT, miR‐485‐5p, and CXCL10 was identified. Ectopic expression and depletion assays were implemented in Ang II‐treated mice or HL‐1 cells, or those co‐cultured with serum‐derived EVs to explore the roles of EV‐carried MIAT. Results MIAT was upregulated in EVs from serum samples of AF patients. Further analysis indicated that MIAT enriched in serum‐derived EVs promoted atrial fibrosis, inflammation and oxidative stress, and aggravated the atrial remodeling and resultant AF. Mechanistically, MIAT bound to miR‐485‐5p and weakened its inhibitory role on the target CXCL10, which was responsible for the role of serum‐derived EV containing MIAT in cellular fibrosis, oxidative stress and inflammation, and atrial remodeling in vivo. Conclusions In conclusion, serum‐derived EV containing MIAT facilitates atrial remodeling and exacerbates the AF by abolishing the miR‐485‐5p‐mediated CXCL10 inhibition. This finding aids in the deeper understanding about the pathophysiology of AF.

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The role of long non-coding RNA MIAT in cancers

Cited by 39 publications

References 101 publications

lncRNA MIAT/HMGB1 Axis Is Involved in Cisplatin Resistance via Regulating IL6-Mediated Activation of the JAK2/STAT3 Pathway in Nasopharyngeal Carcinoma

lncRNA MIAT/HMGB1 Axis Is Involved in Cisplatin Resistance via Regulating IL6-Mediated Activation of the JAK2/STAT3 Pathway in Nasopharyngeal Carcinoma

The COX10-AS1/miR-641/E2F6 Feedback Loop Is Involved in the Progression of Glioma

Serum extracellular vesicles containing MIAT induces atrial fibrosis, inflammation and oxidative stress to promote atrial remodeling and atrial fibrillation via blockade of miR‐485‐5p‐mediated CXCL10 inhibition

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