MIR494

Summary

MIR494 (microRNA 494, HGNC:32084) is a microRNA gene on chromosome 14q32.31.

microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop.

Source: NCBI Gene 574452 — RefSeq curated summary.

At a glance

• Gene type: non-coding (miRNA) — 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:32084
Approved symbol	MIR494
Name	microRNA 494
Location	14q32.31
Locus type	RNA, micro
Status	Approved
Aliases	hsa-mir-494
Ensembl gene	ENSG00000194717
Ensembl biotype	miRNA
OMIM	616036
Entrez	574452
RNAcentral	URS00006A5ABA — miRNA, 81 nt, 22 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000349529

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000349529 — 1 exons

Exon	Start	End
ENSE00001398445	101029634	101029714

Expression profiles

Bgee: expression breadth broad, 49 present calls, max score 95.61.

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
adrenal tissue	UBERON:0018303	95.61	gold quality
kidney	UBERON:0002113	85.08	gold quality
primordial germ cell in gonad	CL:0000670 ∩ UBERON:0000991	82.17	gold quality
stomach	UBERON:0000945	80.92	gold quality
monocyte	CL:0000576	79.54	gold quality
placenta	UBERON:0001987	77.82	gold quality
heart	UBERON:0000948	75.82	gold quality
heart left ventricle	UBERON:0002084	74.20	gold quality
intestine	UBERON:0000160	73.72	gold quality
lung	UBERON:0002048	72.02	gold quality
colon	UBERON:0001155	70.41	gold quality
C1 segment of cervical spinal cord	UBERON:0006469	69.96	gold quality
right adrenal gland cortex	UBERON:0035827	69.91	gold quality
left adrenal gland cortex	UBERON:0035825	69.11	gold quality
left adrenal gland	UBERON:0001234	68.24	gold quality
esophagogastric junction muscularis propria	UBERON:0035841	68.00	gold quality
liver	UBERON:0002107	67.41	gold quality
lower esophagus muscularis layer	UBERON:0035833	67.28	gold quality
subcutaneous adipose tissue	UBERON:0002190	66.68	gold quality
ascending aorta	UBERON:0001496	66.22	gold quality
left uterine tube	UBERON:0001303	66.21	gold quality
myometrium	UBERON:0001296	66.01	gold quality
muscle layer of sigmoid colon	UBERON:0035805	65.88	gold quality
Brodmann (1909) area 9	UBERON:0013540	64.84	gold quality
left ovary	UBERON:0002119	64.74	gold quality
body of pancreas	UBERON:0001150	64.50	gold quality
right hemisphere of cerebellum	UBERON:0014890	64.24	gold quality
putamen	UBERON:0001874	64.19	gold quality
body of uterus	UBERON:0009853	64.05	gold quality
amygdala	UBERON:0001876	63.55	gold quality

Single-cell (SCXA)

Detected in 1 experiment(s), a significant marker in 0.

Experiment	Marker?	Max mean expression
E-ANND-3	no	0.49

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

• TEL-AML1 might exert its antiapoptotic action at least in part by suppressing miRNA-494 and miRNA-320a, lowering their expression causing enhanced survivin expression. (PMID:20807887)
• miR-494 is down-regulated in cholangiocaarcinoma and that its up-regulation induces cancer cell growth retardation through multiple targets involved in the G1-S transition (PMID:21809359)
• microRNA 494 and HUR functionally competed for modulation of nucleolin expression. (PMID:21859890)
• microRNAs as negative regulators of the CFTR gene expression (PMID:22028919)
• Findings indicate that miR-494 is a negative regulator of KIT in gastrointestinal stromal tumors (GIST) and overexpressing miR-494 in GISTs may be a promising approach to GIST treatment. (PMID:22042971)
• IGF2BP1 and its downstream target IGF2 could be a crucial axis for miR-494 in regulation of the destiny of A549 lung cancer cells. (PMID:22151897)
• The miR-494 has a global regulatory role in cell cycle progression, exerted by concerted effects on multiple proteins involved in gap 1 (G) to synthesis (S), as described previously, as well as G to M progression. (PMID:22785131)
• In receptive endometrium from fertile women, miR-494 is downregulated. (PMID:22902743)
• Data show a link between the ERK1/2 pathway and BIM expression through miR-494. (PMID:23012423)
• Urinary microRNA-494 levels were 60-fold higher in patients with acute kidney injury than in normal controls. (PMID:23160513)
• Increased expression of miR-145, miR-223, and miR-494 in vivo in bronchial epithelium of individuals carrying the DeltaF508 CFTR mutation correlates with decreased CFTR expression. (PMID:23436935)
• results indicate that angiogenesis induced by radiotherapy is associated with an MMP-9-miR-494-SDC1 regulatory loop (PMID:23728345)
• miR-494 is involved in the mechanism of estrogen-mediated downregulation of PS expression (PMID:23789915)
• overexpressed in hepatocellular carcinoma and aids in transformation by regulating the G1/S cell cycle transition through targeting of the Mutated in Colorectal Cancer tumor suppressor (PMID:23913442)
• It negatively regulates DJ-1 expression that exacerbate neurodegeneration. (PMID:24269020)
• Ectopic expression of p190B suppressed the miR-494-induced EGFR upregulation. (PMID:24316134)
• the present study concludes that the upregulation of miR-494 expression by TNF-alpha-mediated inflammation exacerbates insulin resistance. (PMID:24349514)
• Overexpression of miR-494 upregulated HIF-1alpha expression through activating PI3K/Akt pathway under both normoxia and hypoxia, and had protective effects against hypoxia-induced apoptosis in L02 cells. (PMID:24364919)
• Aberrant expression levels of miR-186, miR-494 and miR-3651 in whole blood samples of oral squamous cell carcinoma are associated with malignancy. (PMID:24452363)
• It acts as an anti-oncogene in gastric carcinoma by targeting c-myc. (PMID:24612089)
• Our results suggested that miR-494-3p might play crucial role in prostate cancer by post-transcriptional regulation to CXCR4 mRNA (PMID:24644030)
• Loss of SMAD4 in PDAC cells leads to reduced levels of miR-494, increased levels of FOXM1, and nuclear localization of beta-catenin in pancreatic ductal adenocarcinoma. (PMID:24859161)
• miR-142-3p and miR-494 may function as cis- and trans-acting signals contributing to local temporal coordination of cell-autonomous circadian clocks (PMID:24928439)
• Data show that in arterial endothelial cells, inhibition of miR-329, miR-487b, and miR-495 all led to increased cell proliferation by approximately 20%, 50%, and 35%, respectively, but inhibition of miR-494 did not affect endothelial cell proliferation. (PMID:25085941)
• findings show CB1 receptors are regulated by miR-494 and CB2 receptors are targeted by miR-665;in chronic heart failure (CHF) miR-665 expression is significantly decreased and miR-494 is slightly increased; results suggest that in CHF, altered expression of specific miRNAs may contribute to a compensatory response of diseased myocardium (PMID:25111814)
• These results suggest SCGN is involved in the chemoresistance of small cell lung cancer under the regulation of miR-494 (PMID:25226615)
• we provided convincing evidence that upregulation of miR-494 was associated with tumor aggressiveness and tumor metastasis and promoted cell migration and invasion by targeting PTEN gene in colorectal cancer. (PMID:25270723)
• Results show that in metastatic breast cancer, up-regulated levels of miR-183, miR-494 and miR-21 were associated with a poor prognosis. (PMID:25277099)
• miR-494 regulates cell growth, invasion and apoptosis of esophageal squamous cell carcinoma cells by targeting CLPTM1L. (PMID:25480402)
• miR-494 repressed the expression of HOXA10 and also reduced the proliferation of oral cancer cells. These data give more evidence of the role of miR-494 as a tumor suppressor miRNA in oral cancer. (PMID:25500095)
• Our results provide an extensive genome wide set of targets for miR-503, miR-103, and miR-494, and suggest that miR-503 may act as a tumor suppressor in breast cancer by its direct non-canonical targeting of DDHD2. (PMID:25653011)
• Human miR-494 arrests cell cycle at G1/S transition and affects mesenchymal stem cells function of secreting VEGF and may be a novel mechanism in the development of preeclampsia. (PMID:25660325)
• miR-494-3p inhibitor could prevent migration, invasion, proliferation, and promote apotosis in gliomas through PTEN/AKT pathway. (PMID:25662849)
• miR-494 expression was significantly upregulated in human cervical cancer cell lines and tissues. miR-494 upregulation was associated with PTEN downregulation. Inhibition of miR-494 suppressed cell proliferation by targeting the 3’-UTR of PTEN mRNA. (PMID:25738254)
• GALNT7 and CDK16 were confirmed to be the direct targets of miR-494. These results suggested that miR-494 play an inhibitory role in the tumorigenesis of NPC (PMID:25809707)
• MicroRNA is up regulated in human hepatocellular carcinoma indicating vascular invasion in patients diagnosed with liver cancer. (PMID:25820676)
• Combined detection of PTEN and miR-494 can aid in determining malignancy degree and the prognosis of patients with non-small cell lung cancer (PMID:25861022)
• miR-494 is directly bound to DPYD 3’UTR and negatively regulated DPYD expression in colon cancer. (PMID:25873402)
• miR-494 is a novel regulator of HNPC apoptosis induced by TNF-alpha (PMID:25906693)
• Findings show that miR-494 is downregulated in breast cancer cells, and is able to suppress cell proliferation, migration and invasion through regulation of Wnt/beta-catenin/CXCR4 pathway suggesting it as a potential therapeutic target for breast cancer. (PMID:25955111)

Cross-species orthologs

2 orthologs

Organism	Symbol	Gene ID
mus_musculus	Mir494	ENSMUSG00000070141
rattus_norvegicus	Mir494	ENSRNOG00000036244

Paralogs (16): MIR377 (ENSG00000199015), MIR381 (ENSG00000199020), MIR369 (ENSG00000199025), MIR323A (ENSG00000199069), MIR410 (ENSG00000199092), MIR409 (ENSG00000199107), MIR539 (ENSG00000202560), MIR487A (ENSG00000207742), MIR487B (ENSG00000207754), MIR656 (ENSG00000207959), MIR496 (ENSG00000207961), MIR154 (ENSG00000207978), MIR323B (ENSG00000208004), MIR1185-1 (ENSG00000221525), MIR1185-2 (ENSG00000221614), MIR382 (ENSG00000283170)

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.