MIR16-1

gene
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Also known as hsa-mir-16-1

Summary

MIR16-1 (microRNA 16-1, HGNC:31545) is a microRNA gene on chromosome 13q14.2.

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 406950 — 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:31545
Approved symbolMIR16-1
NamemicroRNA 16-1
Location13q14.2
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-16-1
Ensembl geneENSG00000208006
Ensembl biotypemiRNA
OMIM609704
Entrez406950
RNAcentralURS000056BFD0 — miRNA, 89 nt, 26 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385271

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385271 — 1 exons

ExonStartEnd
ENSE000015002775004897350049061

Expression profiles

Bgee: expression breadth broad, 37 present calls, max score 80.65.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
bloodUBERON:000017880.65gold quality
heartUBERON:000094878.04gold quality
lungUBERON:000204873.71gold quality
gastrocnemiusUBERON:000138872.85gold quality
stomachUBERON:000094572.07gold quality
body of stomachUBERON:000116171.99gold quality
right atrium auricular regionUBERON:000663169.93gold quality
lower esophagus muscularis layerUBERON:003583369.55gold quality
body of pancreasUBERON:000115068.93gold quality
ascending aortaUBERON:000149668.05gold quality
tibial arteryUBERON:000761067.64gold quality
upper lobe of left lungUBERON:000895267.16gold quality
transverse colonUBERON:000115766.64gold quality
skin of abdomenUBERON:000141665.89gold quality
vaginaUBERON:000099665.74gold quality
small intestine Peyer’s patchUBERON:000345465.52gold quality
body of uterusUBERON:000985365.50gold quality
zone of skinUBERON:000001465.49gold quality
esophagus mucosaUBERON:000246965.15gold quality
skin of legUBERON:000151164.73gold quality
subcutaneous adipose tissueUBERON:000219064.61gold quality
esophagogastric junction muscularis propriaUBERON:003584164.04gold quality
prostate glandUBERON:000236762.74gold quality
omental fat padUBERON:001041462.45gold quality
left adrenal gland cortexUBERON:003582561.89gold quality
ectocervixUBERON:001224961.77gold quality
adenohypophysisUBERON:000219661.22gold quality
cerebellar hemisphereUBERON:000224560.98gold quality
minor salivary glandUBERON:000183060.73gold quality
spleenUBERON:000210660.22gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.94

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • BCL2 repression by miR-16 induces apoptopsis in a leukemic cell line model. (PMID:16166262)
  • high-throughput profiling of genes modulated by miR-15a/16-1 in a leukemic cell line model (MEG-01) and in primary CLL samples (PMID:18362358)
  • Human miR-16 microRNA could play a role in the development of MDR in gastric cancer cells at least in part by modulation of apoptosis via targeting BCL2. (PMID:18449891)
  • miR-16-1 regulates CCND1 mRNA expression; role of miR-16-1 in the regulation of CCND1 in MCL (PMID:18483394)
  • restoration of c-Myb levels partly alleviates tumors suppressive effects of miR-15a/16, suggesting that c-Myb is a key downstream target of this microRNA cluster (PMID:18708755)
  • Rheumatoid arthritis peripheral blood mononuclear cells exhibited increases in miR-146a, miR-155, miR-132, and miR-16 expression, whereas let-7a expression was not significantly different compared with healthy control individuals. (PMID:18759964)
  • HNRNP K and microRNA-16 have roles in cyclooxygenase-2 RNA stability induced by S100b, a ligand of the receptor for advanced glycation end products (PMID:18854308)
  • The targeting of miR-16 to a predicted binding site in the VEGF 3’UTR was validated; miR-16 regulates expression of endogenous VEGF. (PMID:19144909)
  • the myeloid-specific miR-223 and the apoptosis and cell cycle arrest-inducing miR15 ~ 16 clusters were regulated by glucocorticoids in acute lymphoblastic leukemia (PMID:19148136)
  • MiR-16 negatively regulate HMGA1 and caprin-1 which are involved in cell proliferation. (PMID:19250063)
  • propose that the underlying pathomechanism of CLL involves co-regulation of miRNA genes miR-16-1 and miR-15a by the two long non-coding RNA genes DLEU1 and DLEU2. (PMID:19347735)
  • microRNA-16 regulates proliferation and growth of MM cells in vitro and in vivo by inhibiting AKT serine/threonine-protein-kinase (AKT3), ribosomal-protein-S6, MAP-kinases, and NF-kappaB-activator MAP3KIP3. MIR16. (PMID:19401561)
  • MicroRNAs (miRNAs) encoded by the miR-15/16 cluster are known to act as tumor suppressors (PMID:19498445)
  • analysis of the targets of MIR-15a and MIR-16-1 in patients with chronic lymphocytic leukemia (PMID:19779621)
  • Data show that miR-15a in BM and miR-16 in PB were differentially expressed between low-risk and high-risk groups, while miR-222 and miR-181a expression was higher in AML than in MDS in both BM and PB. (PMID:19883312)
  • miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression. (PMID:20060366)
  • Down-regulation of microRNA 16-1 is associated with malignant pheochromocytomas. (PMID:20621999)
  • important role of miR-16 in regulating HuR translation and the link of this regulatory pathway to human breast cancer. (PMID:20626035)
  • miR-16, miR-21, and miR-146a were significantly downregulated in cigarette smoke-exposed placentas compared to controls and associated with adverse pregnancy outcomes. (PMID:20647767)
  • The mechanism of HER2Delta16 therapeutic evasion, involving tamoxifen-induced upregulation of BCL-2 and suppression of miR-15a/16. (PMID:20876285)
  • Data indicate an inverse correlation between miR-16-1, miR-181a, miR-181b, and level of expression of TCL-1 and BCL-2, which suggest that these miRNAs may implicate in negatively regulating target mRNA at transcriptional level. (PMID:21130495)
  • Data suggest that miR-15a, -16-1, and MYB may be important therapeutic targets to increase HbF levels in patients with sickle cell disease and beta-thalassemia. (PMID:21205891)
  • mdr1 expression enhanced radiation-induced apoptosis in HepG2 cells, SK-HEP-1 cells, MiHa cells, and furthermore, induced miR-16 and suppressed its target gene Bcl-2 in HepG2 cells. (PMID:21336967)
  • The elevated expression levels of miR-146a and miR-16 are correlated to rheumatoid arthritis disease activity. (PMID:21354921)
  • High levels of MIR16 is associated with non-small-cell lung cancer. (PMID:21400525)
  • our data identify the miR-15 and miR-16 families as novel transcriptional targets of E2F, which, in turn, modulates E2F activity. (PMID:21454377)
  • miR-16-1, are homozygously deleted in a subset of prostate cancers (PMID:21472816)
  • Data provide support to the development of therapies aimed at reconstituting miR-15 and miR-16 in advanced prostate cancer. (PMID:21532615)
  • miR-34a and miR-15a/16 act synergistically to induce cell cycle arrest in a Rb-dependent manner (PMID:21575235)
  • Let-7a and miR-16 plasma levels can serve as noninvasive prognostic markers in MDS patients. (PMID:21602527)
  • Hypoxia-microRNA-16 downregulation induces VEGF expression in anaplastic lymphoma kinase-positive anaplastic large-cell lymphomas. (PMID:21778999)
  • MicroRNA-16 and microRNA-424 regulate cell-autonomous angiogenic functions in endothelial cells via targeting vascular endothelial growth factor receptor-2 and fibroblast growth factor receptor-1. (PMID:21885851)
  • The findings highlighted the role of HDAC3 in Myc-induced miR-15a/16-1 changes and reveal novel mechanisms for c-Myc-driven microRNA suppression and malignant transformation in aggressive B-cell malignancies. (PMID:22002311)
  • Nucleolin protein interacts with microprocessor complex to affect biogenesis of microRNAs 15a and 16 (PMID:22049078)
  • HuR inhibits microRNA-16 targeting of COX-2. (PMID:22049153)
  • Histone deacetylases mediate the silencing of miR-15a, miR-16, and miR-29b in chronic lymphocytic leukemia. (PMID:22096249)
  • These data suggest that miR-15a/16-1 may function as a tumor suppressor to regulate leukemic cell proliferation potentially by down-regulating the WT1 oncogene. (PMID:22133358)
  • Data indicate that miR-15a, miR-16, miR-26ab, miR-196ab and Let-7a as potential HMGA1 and HMGA2-targeting microRNAs. (PMID:22139073)
  • Adenosine A2A receptor upregulation in human PMNs is controlled by miRNA-214, miRNA-15, and miRNA-16 (PMID:22249219)
  • miR-16 targets SMRT and modulates NF-kappaB-regulated transactivation of the IL-8 gene. (PMID:22292036)

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.