MIR182

gene
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Also known as hsa-mir-182miR-182

Summary

MIR182 (microRNA 182, HGNC:31553) is a microRNA gene on chromosome 7q32.2.

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 406958 — 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

FieldValue
HGNC IDHGNC:31553
Approved symbolMIR182
NamemicroRNA 182
Location7q32.2
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-182, miR-182
Ensembl geneENSG00000207990
Ensembl biotypemiRNA
OMIM611607
Entrez406958
RNAcentralURS000075B66E — miRNA, 110 nt, 1 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385255

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385255 — 1 exons

ExonStartEnd
ENSE00001500261129770383129770492

Expression profiles

Bgee: expression breadth broad, 28 present calls, max score 85.25.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
monocyteCL:000057685.25gold quality
body of pancreasUBERON:000115084.16gold quality
bloodUBERON:000017879.74gold quality
lungUBERON:000204874.61gold quality
islet of LangerhansUBERON:000000673.59gold quality
esophagus mucosaUBERON:000246971.70gold quality
muscle layer of sigmoid colonUBERON:003580571.48gold quality
body of stomachUBERON:000116170.65gold quality
right lobe of liverUBERON:000111469.90gold quality
omental fat padUBERON:001041467.83gold quality
transverse colonUBERON:000115767.81gold quality
right adrenal glandUBERON:000123366.76gold quality
body of uterusUBERON:000985366.60gold quality
dorsolateral prefrontal cortexUBERON:000983465.73gold quality
skin of legUBERON:000151165.56gold quality
skin of abdomenUBERON:000141665.29gold quality
prostate glandUBERON:000236764.84gold quality
thoracic mammary glandUBERON:000520064.78gold quality
nucleus accumbensUBERON:000188263.89gold quality
subcutaneous adipose tissueUBERON:000219062.65gold quality
pituitary glandUBERON:000000761.07gold quality
renal glomerulusUBERON:000007460.43silver quality
cerebellar hemisphereUBERON:000224558.83gold quality
epididymisUBERON:000130155.15silver quality
placentaUBERON:000198754.07gold quality
right testisUBERON:000453451.95gold quality
right frontal lobeUBERON:000281051.27gold quality
left testisUBERON:000453349.38gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.16

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • expression of miR-182 increases with progression from primary to metastatic melanoma and inversely correlates with FOXO3 and microphthalmia-associated transcription factor levels (PMID:19188590)
  • Suppression of miR-27a, miR-96, and miR-182 resulted in an increase in FOXO1 expression. (PMID:19574223)
  • miR-21, miR-182 and let7-5a were over-expressed, and miR-145 and miR-155 were under-expressed in a breast, a prostate, and a glioblastoma cancer cell line. (PMID:20370992)
  • ectopic expression of hsa-mir-182 significantly inhibits lung cancer cell proliferation and anchorage-independent cell growth, which can be rescued by re-expression of RGS17. (PMID:20420807)
  • study reports expression of miR-182 was markedly up-regulated in glioma cell lines and in primary glioma specimens; suggests miR-182 could be a valuable marker of glioma progression and high miR-182 expression is associated with poor overall survival (PMID:20472885)
  • data indicate that abnormal processing of pre-miR-182 in patients carrying the T allele of the rs76481776 polymorphism may contribute to the dysregulation of circadian rhythms in major depression patients with insomnia (PMID:20656788)
  • MIR-182-mediated downregulation of BRCA1 impedes DNA repair . (PMID:21195000)
  • Endogenous mature miR-182 expression may have an important role in the pathogenesis of lung cancer through its interference with the target gene CTTN by epigenetic modification. (PMID:21503569)
  • miR-183-96-182 cluster is overexpressed in prostate tissue and regulates zinc homeostasis in prostate cells. (PMID:22045813)
  • High MIR182 is associated with basal breast cancer cells. (PMID:22086602)
  • This study provides both in vitro and in vivo evidence for an important role of miR-182 in leptomeningeal spread of non-SHH–medulloblastoma. (PMID:22134538)
  • Our findings suggest that miR-182 dys-regulation confers powerful oncogenic potential in the tumourigenesis of high-grade serous ovarian carcinoma. (PMID:22322863)
  • These results indicate that miR-182 targets the CREB1 gene and suppresses gastric adenocarcinoma cell growth, suggesting that miR-182 shows tumor-suppressive activity in human gastric cancer. (PMID:22325466)
  • Results show that miR-182 is involved in glucocorticoid resistance, via FOXO3A, and suggest that restoration of miR-182 is a potentially promising therapeutic strategy in lymphoblastic malignancies. (PMID:22582938)
  • Compared with normal tissue, miR-182 was up-reg’d and MTSS1 was down-reg’d in HCC tissues. Over-expression of miR-182 was correlated with intrahepatic metastasis. There was a negative correlation between miR-182 and MTSS1 expression in both HCC tissues. (PMID:22681717)
  • MIR182 expression is significantly higher in high-grade serous ovarian carcinoma than in fallopian tubes. (PMID:22790015)
  • miR-182, a p53 dependent miRNA, suppressed the expression of MITF, BCL2, cyclin D2 and functioned as a potent tumor suppressor in uveal melanoma cells. (PMID:22848417)
  • miR-182 was overexpressed in gliomas & suppressed CYLD, promoting ubiquitin conjugation of NF-kappaB pathway components & an aggressive phenotype in vitro & in vivo. (PMID:23006329)
  • deregulated expression of miR-9, miR-31, and miR-182 during carcinogenesis plays a significant role in the development of colon cancer by promoting proliferation and tumor cell survival. (PMID:23019418)
  • MiR-182 significantly inhibited NAMPT protein expression by acting on the 3’-UTR of the NAMPT mRNA. (PMID:23153509)
  • High miR-182 expression is associated with aggressiveness of muscle-invasive bladder cancer. (PMID:23169479)
  • miR-182-5p plays an important role as an oncogene by knocking down RECK and Smad4, resulting in activation of the Wnt-beta-catenin signaling pathway in bladder cancer. (PMID:23226455)
  • Further examination indicated that only the inhibition of microRNA-182 and/or microRNA-96 rescued the expression of forkhead box O3 inhibited by leptin, and their mimics promoted the proliferation of ovarian cancer cells (PMID:23262295)
  • PDCD4 Is Down-Regulated, Whereas miR-182 Is Up-Regulated in Ovarian Cancer (PMID:23296900)
  • miR-182 plays an onco-miRNA role in cervical cancer and its alteration is associated with cervical cancer pathogenesis by disrupting cell proliferation. (PMID:23313739)
  • GNA13 is an important mediator of prostate cancer cell invasion, and miR-182 and miR-200 family members regulate its expression post-transcriptionally (PMID:23329838)
  • data demonstrate for the first time that miR-182 expression is controlled by beta-catenin (PMID:23333633)
  • miR-182 and miR-203 induce mesenchymal to epithelial transition features and growth factor independent growth via repressing SNAI2 in prostate cells. (PMID:23354685)
  • MicroRNA-182-5p promotes cell invasion and proliferation by down regulating FOXF2, RECK and MTSS1 genes in human prostate cancer. (PMID:23383207)
  • High miRNA-182 expression is associated with triple-negative breast cancer. (PMID:23430586)
  • MiR-182 was up-regulated in colorectal cancer tissues and correlated with adverse clinical characteristics and poor prognosis. (PMID:23474644)
  • In breast tumor samples, miR-182 induction is linked to downregulation of MIM, RhoA activation and poor prognosis. (PMID:23474751)
  • Both miR-146a and miR-182 placental expression patterns are positively associated with subsequent infant quality of movement score. (PMID:23783433)
  • The results suggest that miR-182 plays an important role in the proliferation of human prostate cancer cells by directly suppressing the tumor supressor gene NDRG1. (PMID:23874837)
  • Downregulation of microRNA-182 inhibits cell growth and invasion by targeting programmed cell death 4 in human lung adenocarcinoma cells. (PMID:23877371)
  • although the functional sequence variants in the miR-183-96-182 cluster directly involved in ADHD remain unknown, we have identified a tentative association between this genomic region and ADHD without comorbid SUD. (PMID:23906647)
  • The suppressor activity of miR-182 on ENTPD5 gene was identified for the first time in human colorectal cancer. (PMID:23987127)
  • Tumor-targeting TRAIL expression mediated by miRNA response elements suppressed growth of uveal melanoma cells. (PMID:24001901)
  • MiR-182 promotes cell proliferation and colony formation via TCEAL7 regulation of NFkappaB activity and c-Myc and cyclin D1 expression. (PMID:24021963)
  • Anti-miR-182 could be used to restore TSP-1 expression in order to contrast angiogenic and invasive events in CRC (PMID:24053448)

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.

No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.