MIR122

gene
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Also known as hsa-mir-122ahsa-mir-122miR-122

Summary

MIR122 (microRNA 122, HGNC:31501) is a microRNA gene on chromosome 18q21.31.

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 406906 — 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:31501
Approved symbolMIR122
NamemicroRNA 122
Location18q21.31
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-122a, hsa-mir-122, miR-122
Ensembl geneENSG00000284440
Ensembl biotypemiRNA
OMIM609582
Entrez406906
RNAcentralURS000075E935 — miRNA, 85 nt, 8 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385044

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385044 — 1 exons

ExonStartEnd
ENSE000015000515845107458451158

Expression profiles

Bgee: expression breadth tissue_specific, 2 present calls, max score 98.70.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
liverUBERON:000210798.70gold quality
midbrainUBERON:000189197.83gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.00

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): CEBPA, HNF4A, MYC, ONECUT1, TFDP2

Literature-anchored findings (GeneRIF, showing 40)

  • cyclin G1 is a target of miR-122a in human hepatocellular carcinoma (PMID:17616664)
  • micro-RNA-122 (miR-122) plays an important role in the regulation of hepatitis C virus replication and heme oxygenase-1/Bach1 expression in hepatocytes. (PMID:17919492)
  • although miR-122 is not absolutely required, it greatly enhances HCV replication in nonhepatic cells (PMID:18550664)
  • Bcl-w is a direct target of miR-122 that functions as an endogenous apoptosis regulator in these human hepatocellular carcinoma -derived cell lines. (PMID:18692484)
  • Sequestration of miR-122 in liver cell lines strongly reduces HCV translation, whereas addition of miR-122 stimulates HCV translation in liver cell lines as well as in the non-liver HeLa cells and in rabbit reticulocyte lysate. (PMID:19020517)
  • The binding site requirements for miR-122 to positively regulate hepatitis C virus replication provide an insight into this unusual mode of miRNA action. (PMID:19021529)
  • Decreased levels of microRNA miR-122 in individuals with hepatitis C responding poorly to interferon therapy. (PMID:19122656)
  • miR-122, a tumor suppressor microRNA affecting hepatocellular carcinoma intrahepatic metastasis by angiogenesis suppression, exerts some of its action via regulation of ADAM17. (PMID:19296470)
  • Hepatocellular carcinoma has obvious alteration in the expression patterns of miR-122 and miR-224. (PMID:19403413)
  • Results show that in patients resected for HCC, lower miR-122 levels were associated with a shorter TTR, whereas higher cyclin G1 expression was related to a lower survival, suggesting that miR-122 might represent an effective molecular target for HCC. (PMID:19584283)
  • The down-regulation of miR-122a mediated by aberrant APC/beta-catenin signaling is important to the pathogenesis of gastrointestinal cancers. (PMID:19607815)
  • miR-122 is a marker of hepatocyte-specific differentiation and an important determinant in the control of cell migration and invasion. (PMID:19617899)
  • miR-122 modulates viral RNA abundance independently of its effect on isoprenoid metabolism (PMID:19846523)
  • Aberrant expression of miR-122 may contribute to hepatocarcinogenesis. (PMID:19891584)
  • the insertion/deletion polymorphism at miRNA-122-binding site in the interleukin-1alpha 3’ untranslated region confers risk for hepatocellular carcinoma (PMID:19917630)
  • miR-370 acting via miR-122 may have a causative role in the accumulation of hepatic triglycerides by modulating initially the expression of SREBP-1c, DGAT2, and Cpt1alpha. (PMID:20124555)
  • Downregulation of miR-122 was associated with neoplasms through induction of Bcl-W and/or CCNG1. (PMID:20150764)
  • miR-122a and miR-422a may destabilize CYP7A1 mRNA to inhibit CYP7A1 expression. (PMID:20351063)
  • Human Argonaute 2 targets cap-binding protein80/20-bound mRNAs and exon junction complex-bound mRNAs and inhibits nonsense-mediated mRNA decay which is restricted tightly to CBP80/20-bound mRNAs. (PMID:20395958)
  • Hepatitis C virus RNA with base substitutions in both miR-122 binding sites failed to produce infectious virus in transfected cells, while virus production was rescued to near-wild-type levels in cells supplemented with a complementary miR-122 mutant. (PMID:20427538)
  • These results indicate that miR-122 can exert direct antiviral function by inhibiting Borna disease virus translation and replication on one hand, while acting indirectly through interferon to increase the host innate immunity on the other hand. (PMID:20561966)
  • miR-122 expression inversely correlated with fibrosis, liver transaminase levels and patient age. miR-21 was induced approximately twofold, and miR-122 was downregulated on infection of cultured cells with the HCV J6/JFH, thus establishing a link to HCV. (PMID:20625373)
  • results are consistent with miR-122 acting at an alternative step in the hepatitis C virus life cycle, promoting cap-independent viral translation, enhancing viral RNA stability, or facilitating de novo initiation of viral RNA synthesis (PMID:20637242)
  • miR-122 regulates mitochondrial metabolism and its loss may be detrimental to sustaining critical liver function and contribute to morbidity and mortality of liver cancer patients. (PMID:20739924)
  • proteomic profiling used to identify the target proteins of miR-122a in hepatocellular carcinoma; PRDXII was identified to be the new target of miR-122a (PMID:20859956)
  • significant up-regulation of miRNA-122 between pituitary carcinomas and adenomas (PMID:20960104)
  • Ago2 was necessary for efficient miR-122 enhancement of hepatitis C virus RNA accumulation and translation. (PMID:21177824)
  • Study reports competing roles of the stimulatory microRNA-122 recognition elements (MREs) in the 5’UTR with the inhibitory role of an MRE in the open reading frame to bind hepatitis C virus RNA. (PMID:21185047)
  • In contrast with in vitro findings, hepatic miR-122 expression is not correlated with HCV load in the human liver, but is inversely correlated with both functional and histopathological liver damage. (PMID:21199296)
  • miR-21, miR-122 and miR-223 are elevated in patients with hepatocellular carcinoma (HCC) or chronic hepatitis and these miRNAs have strong potential to serve as novel biomarkers for liver injury but not specifically for HCC. (PMID:21229610)
  • MicroRNA-122 antagonism against hepatitis C virus genotypes 1-6 and reduced efficacy by host RNA insertion or mutations in the HCV 5’ UTR. (PMID:21383155)
  • Two-tiered approach identifies a network of cancer and liver disease-related genes regulated by miR-122 (PMID:21402708)
  • The CPEB 3’ UTR contains two miR-122 binding sites, which when deleted, elevate mRNA translation, as does an antagomir of miR-122 (PMID:21478871)
  • miRNA122a-mediated antigen silencing induced significantly higher anti-HBsAg antibody titers allowing an up to 100-fold vector dose reduction. (PMID:21556053)
  • our study revealed that a number of miRNAs were differentially expressed during HBV infection and underscored the potential importance of miR-122 in the infection process. (PMID:21692939)
  • miR-122 plays an important role in HBV-related hepatocarcinogenesis by targeting NDRG3. (PMID:21725618)
  • Modulation of the unfolded protein response is the core of microRNA-122-involved sensitivity to chemotherapy in hepatocellular carcinoma. (PMID:21750653)
  • TNF-alpha regulates intestinal tight junction permeability by inducing miR-122a-mediated degradation of occludin mRNA. (PMID:21763238)
  • reveal that replication of hepatitis C virus (HCV) RNA depends on recruitment of Ago2 and miRNA-122 to lipid droplets, while suppression of HCV RNA by siRNA and Ago2 involves interaction with P-bodies (PMID:21868483)
  • miR-122 may down-regulate HBV replication by binding to the viral target sequence, contributing to the persistent/chronic infection of HBV, and HBV-induced modulation of miR-122 expression may represent a mechanism to facilitate viral pathogenesis (PMID:21903935)

Cross-species orthologs

2 orthologs

OrganismSymbolGene ID
danio_reriomir122ENSDARG00000083634
mus_musculusMir122ENSMUSG00000065402

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.

  • Disease cohort memberships (association, not causation — diseases whose associated-gene cohort lists this gene; a subset are also under Associated diseases): isolated microphthalmia 3