MIAT

Summary

MIAT (myocardial infarction associated transcript, HGNC:33425) is a long non-coding RNA gene on chromosome 22q12.1.

This gene encodes a spliced long non-coding RNA that may constitute a component of the nuclear matrix. Altered expression of this locus has been reported to be associated with a susceptibility to myocardial infarction. It has also been proposed that pathways involving this transcript may contribute to the pathophysiology of schizophrenia. A similar gene in mouse has been associated with retinal cell fate determination. Alternatively spliced transcript variants have been identified.

Source: NCBI Gene 440823 — RefSeq curated summary.

At a glance

• Gene type: non-coding (lncRNA) — no protein product; not a drug target. Variant/disease associations are omitted (they would be positional, from an overlapping protein-coding gene).

Identifiers

Gene identifiers

Field	Value
HGNC ID	HGNC:33425
Approved symbol	MIAT
Name	myocardial infarction associated transcript
Location	22q12.1
Locus type	RNA, long non-coding
Status	Approved
Aliases	FLJ25967, Rncr2, gomafu, NCRNA00066, LINC00066, lncRNA-MIAT
Ensembl gene	ENSG00000225783
Ensembl biotype	lncRNA
OMIM	611082
Entrez	440823
RNAcentral	URS00026A259D — lncRNA, 10078 nt, 1 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 50 — 50 lncRNA

ENST00000413665, ENST00000418918, ENST00000419237, ENST00000421867, ENST00000422403, ENST00000425476, ENST00000430483, ENST00000436238, ENST00000439738, ENST00000440347, ENST00000449717, ENST00000450203, ENST00000451141, ENST00000452429, ENST00000453023, ENST00000455640, ENST00000458302, ENST00000613780, ENST00000616213, ENST00000616469, ENST00000620145, ENST00000643002, ENST00000643270, ENST00000656640, ENST00000660931, ENST00000665574, ENST00000668051, ENST00000669142, ENST00000670887, ENST00000693710, ENST00000717175, ENST00000717176, ENST00000717177, ENST00000717178, ENST00000717187, ENST00000717188, ENST00000717189, ENST00000717190, ENST00000717191, ENST00000717198, ENST00000717199, ENST00000717200, ENST00000717201, ENST00000717202, ENST00000717208, ENST00000717209, ENST00000717210, ENST00000717211, ENST00000717212, ENST00000718024

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000413665 — 3 exons

Exon	Start	End
ENSE00001673514	26665531	26666220
ENSE00001708395	26657458	26657654
ENSE00001718108	26663316	26663509

Expression profiles

Bgee: expression breadth ubiquitous, 213 present calls, max score 99.04.

FANTOM5 (CAGE): breadth broad, TPM avg 25.6026 / max 1971.4651, expressed in 625 samples.

FANTOM5 promoters (12 alternative TSS)

Promoter ID	TPM avg	Samples expressed
191521	12.6831	534
191522	8.1476	453
191519	2.5457	252
191520	0.8564	201
209433	0.4438	139
191515	0.3344	86
191516	0.1362	53
191518	0.1140	39
191514	0.1096	46
191528	0.1077	54

Top tissues by expression

247 total, by Bgee expression score (0-100, higher = more expressed):

Tissue	Anatomy ID	Expression score	Quality
primary visual cortex	UBERON:0002436	99.04	gold quality
middle temporal gyrus	UBERON:0002771	98.79	gold quality
Brodmann (1909) area 23	UBERON:0013554	98.77	gold quality
occipital lobe	UBERON:0002021	98.65	gold quality
superior frontal gyrus	UBERON:0002661	97.88	gold quality
postcentral gyrus	UBERON:0002581	97.73	gold quality
parietal lobe	UBERON:0001872	97.59	gold quality
Brodmann (1909) area 46	UBERON:0006483	97.18	gold quality
cortical plate	UBERON:0005343	96.10	gold quality
right frontal lobe	UBERON:0002810	96.04	gold quality
lateral nuclear group of thalamus	UBERON:0002736	95.91	gold quality
dorsolateral prefrontal cortex	UBERON:0009834	95.90	gold quality
Brodmann (1909) area 9	UBERON:0013540	95.86	gold quality
pituitary gland	UBERON:0000007	95.00	gold quality
ganglionic eminence	UBERON:0004023	94.52	gold quality
entorhinal cortex	UBERON:0002728	94.16	gold quality
anterior cingulate cortex	UBERON:0009835	94.10	gold quality
lateral globus pallidus	UBERON:0002476	93.48	gold quality
nucleus accumbens	UBERON:0001882	93.13	gold quality
superior vestibular nucleus	UBERON:0007227	93.04	gold quality
cerebral cortex	UBERON:0000956	92.94	gold quality
hypothalamus	UBERON:0001898	92.67	gold quality
forebrain	UBERON:0001890	92.63	gold quality
adenohypophysis	UBERON:0002196	92.62	gold quality
granulocyte	CL:0000094	92.46	gold quality
temporal lobe	UBERON:0001871	92.21	gold quality
ventral tegmental area	UBERON:0002691	92.19	gold quality
neocortex	UBERON:0001950	92.08	gold quality
substantia nigra pars compacta	UBERON:0001965	91.80	gold quality
frontal cortex	UBERON:0001870	91.35	gold quality

Single-cell (SCXA)

Detected in 3 experiment(s), a significant marker in 3.

Experiment	Marker?	Max mean expression
E-HCAD-35	yes	92.12
E-HCAD-25	yes	85.53
E-ANND-3	yes	8.60

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

• identification of SNPs in a novel non-coding gene, MIAT, that are associated with increased risk of myocardial infarction. (PMID:17066261)
• These results functionally link activity-regulated lncRNAs and alternative splicing in neuronal function and suggest that their dysregulation may contribute to neurological disorders. (PMID:23628989)
• Gomafu indirectly modulates the function of the splicing factors SF1 and Celf3 by sequestering these proteins into separate nuclear bodies. (PMID:25145264)
• lncRNA-MIAT expression is increased in diabetic retinas. MIAT is a competing endogenous RNA, forming a feedback loop with VEGF and miR-150-5p to regulate endothelial cell function. (PMID:25587098)
• Study revealed that rs1894720 in lncRNA MIAT was significantly associated with paranoid schizophrenia in the Chinese Han population, and the minor allele T contributed to increased disease risk with an odds ratio of 1.48 in a large combined cohort (PMID:26004688)
• Here we review the growing understanding and potential utilization of MIAT (PMID:26707210)
• MIAT acted as a ceRNA, and formed a feedback loop with Akt and miR-150-5p to regulate human lens epithelial cells function. (PMID:26818536)
• A lncRNA (MIAT) is selectively upregulated in neuroendocrine prostate cancers and might interact with Polycomb genes. [review] (PMID:27096814)
• lncRNA MIAT is a potential new biomarker for aggressiveness of chronic lymphocytic leukemia and that MIAT functions to protect malignant mature B cells from cell apoptosis. (PMID:27527866)
• the expression of MIAT was downregulated in a time-dependent manner during human adipose-derived stem cells osteoinduction. (PMID:27797128)
• these findings suggested that MIAT plays an oncogenic role in non-small-cell lung cancer (NSCLC) through the ZEB1 signaling pathway by sponging miR-150, and MIAT may therefore serve as a valuable prognostic biomarker and therapeutic target for NSCLC. (PMID:28843520)
• The results of this study demonstrate the high expression of Gomafu in PBMCs in treatment-naive Schizophrenia. (PMID:28911914)
• Leukocyte expression of MIAT was significantly upregulated in ischemic stroke patients and associated with stroke severity and infarct volume. (PMID:29030044)
• MIAT promotes proliferation and hinders apoptosis in atherosclerosis by regulating miR-181b/STAT3 axis (PMID:29136944)
• results suggest that MIAT involved in breast cancer progression and could be candidate as a novel tumor marker for diagnosis and treatment of breast cancer. (PMID:29345338)
• our study demonstrated that MIAT was upregulated and may function as a ceRNA to increase DDX5 expression by sponging miR-141, which consequently contributed to GC growth and metastasis. (PMID:29540201)
• The interaction of MIAT and miR-133 play a role in the proliferation and metastasis of pancreatic carcinoma. (PMID:29772434)
• Investigated the role of lncRNA MIAT in ER-positive breast cancer cells. MIAT was over-expressed in ER-positive breast cancer tissues and ER-positive breast cancer cell line MCF-7. Mechanistic study identified that MIAT was critical for G1 to S phase cell cycle transition. (PMID:29792859)
• MIAT was an oncogenic lncRNA that promoted proliferation and metastasis of clear cell renal cell carcinoma, and competitively Binding of miR-29c with MIAT and Loxl2. (PMID:30041179)
• The rs1894720 SNP played an important role in age-related hearing loss by regulating the expression of lncRNA MIAT. MIAT could elevate the expression of SIRT1/PGC-1alpha via downregulating miR-29b. And the downregulated SIRT/PGC-1alpha increased the incidence of age-related hearing loss via promoting the apoptosis of cochlear hair cells. (PMID:30556210)
• This study provided mechanistic insights into a critical role for MIAT as a miRNA sponge in chronic pancreatitis. (PMID:30582203)
• The overexpression of myocardial infarction associated transcript (MIAT) in melanoma promotes cell proliferation, cell invasion and migration. MIAT significantly upregulates the phosphorylation of phosphatidylinositol 3-kinases and proto-oncogene proteins c-akt and promotes cMyc and cyclin D1 protein expression. (PMID:30614798)
• High MIAT expression is associated with osteosarcoma progression. (PMID:30629798)
• Taken together, the studied lncRNAs MALAT1, MIAT, and ANRIL might be implicated in beta-thal pathogenesis and could provide new molecular biomarkers for beta-thalassemia after validation in large-scale future studies. (PMID:30665334)
• MIAT was significantly upregulated in serum of patients with symptoms of atherosclerotic vulnerable plaque. These data also demonstrated how MIAT inhibited efferocytosis by targeting miR-149-5p/CD47 axis. (PMID:30755588)
• VEGF stimulation promoted cell proliferation and migration of HUVECs mainly through regulating MIAT/miR-1246/ACE. (PMID:30782069)
• Differentially expressed lncRNA myocardial infarction associated transcripts (MIAT) were highly expressed in patients with multiple myeloma (MM) and were predictive of poor survival outcomes. Moreover, MIAT expression was significantly increased in bortezomib-resistant patients with MM compared with newly diagnosed patients with MM. (PMID:30967527)
• Long noncoding RNA myocardial infarction associated transcript promotes the development of thoracic aortic by targeting microRNA-145 via the PI3K/Akt signaling pathway. (PMID:30989723)
• Upregulated MIAT promoted epithelial-mesenchymal transition of tongue squamous cell carcinoma cells through activation of Wnt/beta-catenin signaling pathway and indicated a poor prognosis (PMID:31166624)
• Repression of miR-212 partly abrogated the inhibitory effects of MIAT knockdown on papillary thyroid cancer cells. (PMID:31404776)
• lncRNA miat functions as a ceRNA to upregulate sirt1 by sponging miR-22-3p in HCC cellular senescence. (PMID:31503007)
• the plasma levels of MIAT were significantly increased in patients with AMI compared with nonAMI patients. (PMID:31661125)
• MIAT is involved in promoting the progression of acute myeloid leukemia (AML), at least partly, through negative regulation of miR-495, and therefore provide a promising target for treatment of AML. (PMID:31698307)
• Association of N(6)-methyladenine DNA with plaque progression in atherosclerosis via myocardial infarction-associated transcripts. (PMID:31797919)
• lncRNA MIAT promotes esophageal squamous cell carcinoma progression by regulating miR-1301-3p/INCENP axis and interacting with SOX2. (PMID:31943174)
• Long non-coding RNA myocardial infarction associated transcript promotes the proliferation of cholangiocarcinoma cells by targeting miR-551b-3p/CCND1 axis. (PMID:32064660)
• Promoter polymorphisms in the lncRNA-MIAT gene associated with acute myocardial infarction in Chinese Han population: a case-control study. (PMID:32090249)
• lncRNA MIAT Regulates Cell Growth, Migration, and Invasion Through Sponging miR-150-5p in Ovarian Cancer. (PMID:32186927)
• Down-regulation of MIAT suppresses osteosarcoma progression by acting as a ceRNA for miR-141-3p to regulate SIX1-mediated PI3K/AKT pathway. (PMID:32196573)
• Long non-coding RNA MIAT promotes cervical cancer proliferation and migration. (PMID:32239132)

Cross-species orthologs

0 orthologs

Protein

Non-coding RNA — no protein product; not a drug target.

Function

No curated pathway, Gene-Ontology, or interaction data.

Disease & clinical

No curated disease, variant, or cancer-driver associations.

Drugs & pharmacology

No drug or pharmacology data — not an established drug target.