MIR23B

gene
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Also known as hsa-mir-23b

Summary

MIR23B (microRNA 23b, HGNC:31606) is a microRNA gene on chromosome 9q22.32.

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 407011 — 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:31606
Approved symbolMIR23B
NamemicroRNA 23b
Location9q22.32
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-23b
Ensembl geneENSG00000207563
Ensembl biotypemiRNA
OMIM610723
Entrez407011
RNAcentralURS0000283D0A — miRNA, 97 nt, 13 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000384832

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000384832 — 1 exons

ExonStartEnd
ENSE000014998399508520895085304

Expression profiles

Bgee: expression breadth ubiquitous, 114 present calls, max score 95.45.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
sural nerveUBERON:001548895.45gold quality
placentaUBERON:000198793.32gold quality
endometriumUBERON:000129591.36gold quality
skeletal muscle tissueUBERON:000113489.76gold quality
olfactory segment of nasal mucosaUBERON:000538687.50gold quality
right lungUBERON:000216786.12gold quality
right coronary arteryUBERON:000162585.47gold quality
descending thoracic aortaUBERON:000234585.40gold quality
ascending aortaUBERON:000149683.25gold quality
thoracic aortaUBERON:000151582.96gold quality
mucosa of stomachUBERON:000119982.69gold quality
uterusUBERON:000099582.65gold quality
muscle of legUBERON:000138382.61gold quality
fundus of stomachUBERON:000116082.54gold quality
skin of abdomenUBERON:000141681.64gold quality
myometriumUBERON:000129681.59gold quality
esophagus mucosaUBERON:000246981.08gold quality
right adrenal glandUBERON:000123380.39gold quality
left uterine tubeUBERON:000130380.36gold quality
esophagusUBERON:000104379.70gold quality
body of pancreasUBERON:000115079.48gold quality
esophagogastric junction muscularis propriaUBERON:003584178.90gold quality
right adrenal gland cortexUBERON:003582778.88gold quality
popliteal arteryUBERON:000225078.81gold quality
tibial arteryUBERON:000761078.77gold quality
zone of skinUBERON:000001478.53gold quality
stomachUBERON:000094578.47gold quality
left coronary arteryUBERON:000162678.42gold quality
lower esophagus muscularis layerUBERON:003583378.04gold quality
lower esophagusUBERON:001347378.01gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no1.45

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • Studies indicate a role for Myc in stimulating glutamine catabolism, in part through the repression of miRNAs miR-23a and miR-23b. (PMID:20086171)
  • MicroRNA-23b plays a role in pulsatile-flow-regulation of retinoblastoma-protein phosphorylation and endothelial cell growth. (PMID:20133741)
  • miR-23b, by targeting proline oxidase, could function as an oncogene. (PMID:20562915)
  • Data show that p15/miR-23b/uPA are involved in HPV-16 E6-associated cervical cancer development. (PMID:21242962)
  • RIG-I signaling results in the inhibitions of infections of rhinoviruses 1B through the miR-23b-mediated down-regulation of its receptor VLDLR (PMID:21642441)
  • MiR-23b, which is downregulated in human colon cancer samples, potently mediates the multiple steps of metastasis, including tumour growth, invasion and angiogenesis in vivo. (PMID:22109528)
  • Over 90% of the analyzed metastatic castration resistant prostate tumors could be characterized by increased miR-221/-222 expression and down-regulated miR-23b/-27b expression. (PMID:22127852)
  • we demonstrated that downregulation of miR-23b suppressed tumor survival through targeting VHL (PMID:22649212)
  • MiR-23b suppresses IL-17-, tumor necrosis factor alpha (TNF-alpha)- or IL-1beta-induced NF-kappaB activation and inflammatory cytokine expression by targeting TAB2, TAB3 and IKK-alpha. (PMID:22660635)
  • the effects of PRDX3 in PCa progression may be caused by the regulation function of miR-23b, and consequently, miR-23b may be involved in the response of PCa cells to hypoxia stress (PMID:22710126)
  • duced expression of miR-23b enhances glioma cell migration in vitro and invasion ex vivo via modulation of Pyk2 protein expression. (PMID:22745829)
  • miR-23b is epigenetically down-regulated and restoration of miR-23b can effectively suppress cell growth in glioma stem cells. (PMID:22982144)
  • Loss of miR-23b may confer proliferative advantage and promote prostate cancer migration and invasion, and reexpression of miR-23b may contribute to the epigenetic therapy for prostate cancer. (PMID:23074286)
  • miR-23b-3p is an oncogenic miRNA and inhibits PTEN tumor suppressor gene in renal cell carcinoma. (PMID:23189187)
  • Downregulation of microRNA -23b is associated with metastatic, castration-resistant prostate tumors. (PMID:23300597)
  • miR-23b and miR-27b are regulated by Her2/Neu, EGF, and TNF-alpha in breast cancer (PMID:23338610)
  • MiR23a and miR23b are potential biomarkers of ovarian endometriosis. (PMID:23450049)
  • MicroRNA-23b functions as a tumor suppressor by regulating Zeb1 in bladder cancer. (PMID:23844063)
  • MicroRNA 23b regulates autophagy associated with radioresistance of pancreatic cancer cells. (PMID:23916944)
  • overexpression of miRNA-23b in U251 cells markedly inhibited the proliferation, cell cycle progression, migration and colony formation, while overexpression of TFAM significantly enhanced these biological processes (PMID:24002170)
  • MIR23B targets the 3’UTR of the autophagy-related gene ATG12, thereby decreasing autophagic activity and ultimately promoting radiation-induced pancreatic cancer cell death. (PMID:24145177)
  • High miR-23b expression is associated with medulloblastoma. (PMID:24203893)
  • Down-regulation of miR-23b was significantly correlated with tumor aggressiveness and poor prognosis of patients with epithelial ovarian cancer. (PMID:24613919)
  • miR-23b and miR-130b downregulation may contribute to pituitary tumorigenesis. (PMID:24681352)
  • Data indicate that peroxiredoxin III (PrxIII) is a common direct target of both miroRNAs miR-26a-5p and miR-23b-3p. (PMID:24828865)
  • Hemodynamic forces modulate EC proliferative phenotype through the miR-23b/CAK/cyclin H pathway. (PMID:24855060)
  • findings support a lung metastasis-promoting function of the miR-23b/27b/24 cluster of miRNAs, which functions in part through the direct inhibition of PSAP in breast cancer (PMID:24966325)
  • Metastatic breast cancer cells in patient bone marrow had increased miR-23b and decreased MARCKS expression. (PMID:24985346)
  • miR-23b and miR-27b function as tumor suppressors, targeting several oncogenic genes in clear cell renal cell carcinoma cells (PMID:25014580)
  • downregulation of the miR-23b/27b/24-1 cluster was a frequent event in prostate cancer, and these clustered miRNAs functioned as tumor suppressors (PMID:25115396)
  • Silencing of the exocytotic RAB family members RAB27A or RAB27B halted miR23b and miR921 secretion and reduced cellular invasion. (PMID:25261234)
  • miR23b has a role in immunity, endothelial function, differentiation, and cancer as well as a potential for translation into future cancer diagnostics and therapeutics [review] (PMID:25301113)
  • We conclude that the decreased expression of the tumor-suppressive miR-23b/27b cluster enhanced cancer cell proliferation, migration and invasion in BC through direct regulation of EGFR and c-Met signaling pathways (PMID:25405368)
  • These results suggest the probability of utilizing miR-23a and miR-23b as therapeutic targets for the treatment of prostate cancer (PMID:25604141)
  • These results suggest that the dysregulation of miR-23a and miR-23b may be implicated in the progression of human gastric cancer (PMID:25674252)
  • MiR-23b promoted cell growth. (PMID:25765901)
  • miR-23b-3p inhibited autophagy mediated by ATG12 and HMGB2 and sensitized GC cells to chemotherapy (PMID:25996293)
  • Results suggest that Notch2 pathway and miR-23b interplay in a reciprocal regulation loop in gastric cancer cells and this axis plays an important role in gastric carcinogenesis. (PMID:26041881)
  • Three miRNAs including hsa-mir-23b, hsa-mir-365-1 and hsa-mir-365-2 showed significant influence on prognosis of Colorectal cancer (PMID:26269151)
  • miR-23b could be a potential prognostic marker for early stage non-small cell lung cancer. (PMID:26314549)

Cross-species orthologs

3 orthologs

OrganismSymbolGene ID
danio_reriodre-mir-23bENSDARG00000081514
danio_rerioMIR23BENSDARG00000081915
mus_musculusMir23bENSMUSG00000065599

Paralogs (1): MIR23A (ENSG00000207980)

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.