MIR96

gene
On this page

Also known as hsa-mir-96

Summary

MIR96 (microRNA 96, HGNC:31648) 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 407053 — 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:31648
Approved symbolMIR96
NamemicroRNA 96
Location7q32.2
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-96
Ensembl geneENSG00000199158
Ensembl biotypemiRNA
OMIM611606
Entrez407053
RNAcentralURS00004E4AD0 — miRNA, 78 nt, 43 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000362288

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000362288 — 1 exons

ExonStartEnd
ENSE00001437051129774692129774769

Expression profiles

Bgee: expression breadth broad, 13 present calls, max score 73.10.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
monocyteCL:000057673.10gold quality
lungUBERON:000204871.24gold quality
bloodUBERON:000017868.93gold quality
endometriumUBERON:000129568.84gold quality
skin of abdomenUBERON:000141665.92gold quality
lower esophagus muscularis layerUBERON:003583364.66gold quality
left ovaryUBERON:000211963.83gold quality
pituitary glandUBERON:000000763.01gold quality
cerebellar hemisphereUBERON:000224559.75gold quality
right frontal lobeUBERON:000281057.00gold quality
placentaUBERON:000198753.75gold quality
islet of LangerhansUBERON:000000652.88gold quality
left testisUBERON:000453343.10gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.06

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • these mutations may alter the regulatory role of miR-96 in maintaining gene expression profiles in hair cells required for their normal function (PMID:19363479)
  • Suppression of miR-27a, miR-96, and miR-182 resulted in an increase in FOXO1 expression. (PMID:19574223)
  • Support a role for VAMP8/endobrevin in the heterogeneity of platelet reactivity, and suggest a role for microRNA-96 in the regulation of VAMP8 expression. (PMID:19943878)
  • Findings identify miR-96 as a potent regulator of KRAS in pancreatic cancer. (PMID:20610624)
  • miR-96 induces cell proliferation in human breast cancer by downregulating transcriptional factor FOXO3a (PMID:21203424)
  • Overexpression of microRNA-96 is associated with inhibition of gamma-globin expression during erythropoiesis. (PMID:21829531)
  • The mRNA and protein levels of insulin receptor substrate 1 (IRS1) and MAP4K1 were significantly reduced in cells transfected with the hsa-miR-96 inhibitor. (PMID:21993544)
  • Even though the mature miR-96 sequence is not altered, we demonstrated that the identified mutation significantly impacts on miR-96 regulation of selected targets. (PMID:22038834)
  • miR-183-96-182 cluster is overexpressed in prostate tissue and regulates zinc homeostasis in prostate cells. (PMID:22045813)
  • MicroRNA 96 is a post-transcriptional suppressor of anaplastic lymphoma kinase expression in cancer cells. (PMID:22414602)
  • Data demonstrated that miR-96, miR-124, and miR-199a regulated the expression of genes important for hMSC differentiation, such as aggrecan, transcription factor SOX9, and fatty acid binding protein 4 (FABP4). (PMID:22441842)
  • Findings indicate that miR-96 regulates DNA repair and chemosensitivity by repressing RAD51 and REV1. (PMID:22761336)
  • did not observe a significant correlation between the expression of miR-96, -145 and -221 and clinicopathologic parameters (PMID:22864280)
  • In conclusion, miR-96 suppresses the expression of forkhead box O1 and forkhead box O3a and promotes the proliferation, migration, and clonogenicity of liver cancer cells. (PMID:23151657)
  • 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)
  • miR-185, miR-96, and miR-223 may repress selective HDL-cholesterol uptake through the inhibition of SR-BI in human hepatic cells. (PMID:23459944)
  • findings suggest that the up-regulation of miR-96 by mitochondrial dysfunction contributes to the development of insulin resistance by targeting IRS-1 in SK-Hep1 cells (PMID:23583389)
  • Overexpression of miR-96 regulates PAX6, which represses neural specification. (PMID:23637338)
  • we found that EVI1 upregulated KRAS expression through suppression of miR-96 in pancreatic cancer cells (PMID:23752186)
  • 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)
  • Upregulation of miR-96 enhances cellular proliferation of prostate cancer cells through FOXO1. (PMID:23951320)
  • miR-96 can regulate apoptosis in prostate cancer, by inhibiting the FOXO1 transcription factor. (PMID:24260486)
  • Data indicate that p21 forms a complex with ZEB1 at the miR-183-96-182 cluster promoter to inhibit transcriptional repression of this cluster by ZEB1, suggesting a reciprocal feedback loop. (PMID:24277930)
  • miR-96 is significantly upregulated in breast cancer. (PMID:24366472)
  • our study demonstrates a novel mechanism of regulation of SMC-specific gene expression and induction of a VSMC contractile phenotype by the BMP4 signaling pathway via suppression of the miR-96-Trb3 axis (PMID:24375867)
  • Our data suggest that miR-96 might promote the growth and motility of NSCLC cells partially by targeting RECK. (PMID:24469470)
  • Inhibition of miR-96 caused expression increase of tumor suppressor gene FOXO1; miR-96 may play a vital role in promoting cell proliferation in human prostate cancer cells (PMID:24633705)
  • Expression of miR-96 was downregulated in newly diagnosed AML patients and associated with leukemic burden, as well as relapse-free survival and overall survival. (PMID:24678958)
  • The miR-96-5p directly inhibits GPC1 to suppress proliferation of pancreatic carcinoma cells. (PMID:24736782)
  • the diurnal rhythm of miR-96-5p may play a role in neuroprotection by regulating neuronal Glutathione levels via the cysteine transporter excitatory amino acid carrier 1. (PMID:24804999)
  • The levels of expression of 25 miRNA remained high and ten of these miRNA showed different expression from that at day 0. (PMID:24960647)
  • HERG1 is identified as a direct target of miR-96, which is downregulated in pancreatic cancer tissues and cell lines. (PMID:25071021)
  • Increased miR-96 levels are associated with idiopathic pulmonary fibrosis. (PMID:25172912)
  • Data indicate that miR-96 suppresses the expression of (nua) kinase family 1 (NUAK1) by targeting its 3’ untranslated region (3’ UTR). (PMID:25242509)
  • MiR-96-5p influences cellular growth of CRC cells. (PMID:25256312)
  • Downregulation of miR-96 inhibits invasion and promotes apoptosis in NSCLC cells A549 and SPC-A-1 by targeting FOXO3 (PMID:25286764)
  • The study found a dose dependent modulation of autophagy by miR-96 through regulation of MTOR and ATG7. (PMID:25333253)
  • MiR-96 reduced the messenger RNA and protein expression levels of tumor protein p53 inducible nuclear protein 1 (TP53INP1), forkhead box protein O1 (FOXO1) and FOXO3a, which are closely associated with cell proliferation. (PMID:25369914)
  • The miR-183/-96/-182 cluster is up-regulated in most breast cancer. It functions as an oncogene in breast cancer as it increases cell proliferation and migration. (PMID:25394902)
  • MIR-96 serves as an oncogene role in esophageal cancer cells through downregulating RECK. (PMID:25465153)

Cross-species orthologs

2 orthologs

OrganismSymbolGene ID
danio_reriodre-mir-96ENSDARG00000083126
mus_musculusMir96ENSMUSG00000065586

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.