MIR34B

gene
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Also known as hsa-mir-34b

Summary

MIR34B (microRNA 34b, HGNC:31636) is a microRNA gene on chromosome 11q23.1.

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 407041 — 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:31636
Approved symbolMIR34B
NamemicroRNA 34b
Location11q23.1
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-34b
Ensembl geneENSG00000207811
Ensembl biotypemiRNA
OMIM611374
Entrez407041
RNAcentralURS0000699DB3 — miRNA, 84 nt, 17 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385076

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385076 — 1 exons

ExonStartEnd
ENSE00001500082111512938111513021

Expression profiles

Bgee: expression breadth broad, 22 present calls, max score 70.61.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
olfactory segment of nasal mucosaUBERON:000538670.61gold quality
skin of abdomenUBERON:000141666.71gold quality
amygdalaUBERON:000187666.44gold quality
lungUBERON:000204865.52gold quality
Ammon’s hornUBERON:000195464.93gold quality
vaginaUBERON:000099664.34gold quality
esophagus mucosaUBERON:000246964.04gold quality
esophagogastric junction muscularis propriaUBERON:003584163.64gold quality
anterior cingulate cortexUBERON:000983562.99gold quality
nucleus accumbensUBERON:000188262.06gold quality
C1 segment of cervical spinal cordUBERON:000646961.44gold quality
tibial nerveUBERON:000132361.36gold quality
lower esophagus muscularis layerUBERON:003583361.10gold quality
thoracic mammary glandUBERON:000520061.08gold quality
hypothalamusUBERON:000189860.95gold quality
thyroid glandUBERON:000204659.57gold quality
left lobe of thyroid glandUBERON:000112058.95gold quality
colonUBERON:000115553.79gold quality
muscle layer of sigmoid colonUBERON:003580553.50gold quality
right testisUBERON:000453451.57gold quality
testisUBERON:000047348.79gold quality
left testisUBERON:000453348.22gold 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

Literature-anchored findings (GeneRIF, showing 40)

  • p53-mediated mir34a, mir34b, and mir34c up-regulation and ING2 down-regulation may be involved in the senescence pathway. (PMID:18451145)
  • miR-34b/c and BTG4 are novel tumor suppressors in colorectal cancer (CRC) and that the miR-34b/c CpG island, which bidirectionally regulates miR-34b/c and BTG4, is a frequent target of epigenetic silencing in CRC (PMID:18519671)
  • evidence for a role of miR-34a and miR-34b/c in the apoptotic response of normal and tumor cells (PMID:19461653)
  • MIR34B regulates TCL1 expression in chronic lymphocytic leukemia (PMID:19536169)
  • Expression of MiR-34s was decreased in tumor samples, and MiR-34 genes underwent minimal deletions and epigenetic inactivation in osteosarcomas. (PMID:19632201)
  • A potentially functional polymorphism in the promoter region of miR-34b/c is associated with an increased risk for primary hepatocellular carcinoma. (PMID:20309940)
  • methylation of miR-34b/c is involved in an epigenetic field defect and that the methylation might be a predictive marker of gastric cancer risk. (PMID:20924086)
  • Downregulation of miR-146b was associated with recurrence and distant metastases in thyroid carcinoma. (PMID:21537871)
  • study to investigate the hypermethylation of miR-34b/c and miR-148a in colorectal cancer, and correlate this data to clinicopathological features; findings show that aberrant hypermethylation of miR-34b/c could be an ideal class of early screening marker (PMID:21610744)
  • Loss of MIRN34B is associated with cell invasion and motility in melanoma. (PMID:21949788)
  • Low expression of MIR34B by DNA hypermethylation was associated with gastric cancers. (PMID:21960261)
  • Frequent MIR34B/C hypermethylation during relapse/progression but not at diagnosis implicated a role of MIR34B/C hypermethylation in myeloma relapse/progression. (PMID:21976676)
  • High microRNA-34b is associated with small-cell lung cancer. (PMID:22047961)
  • data suggest that miR-34b plays a role in the molecular pathogenesis of endometrial cancer (PMID:22052540)
  • DNA methylation of miR-34a, -34b/c, -124-1 and -203 in Philadelphia-negative (Ph-ve) myeloproliferative neoplasms, was studied. (PMID:22082000)
  • MiR-34b expression negatively correlates with disease free survival and overall survival in Triple-negative breast cancer patients (PMID:22439831)
  • In the p53 wild type, KRAS mutated NSCLC cells, the overexpression of miR-34b increases radiosensitivity at low doses of radiation (PMID:22593438)
  • Data indicate that methylation frequency of 5 miR CpG islands (miR-9-1, miR-9-3, miR-137, miR-34b, and miR-210) gradually increased while the proportion of methylated miR-200b gradually decreased during gastric carcinogenesis. (PMID:22703336)
  • miR-34b/c rs4938723CC and TP53 Arg72-Pro polymorphisms may be involved in the susceptibility to intracranial aneurysm. (PMID:22844323)
  • Data suggest that microRNA-34b controls CREB expression and contributes to myeloid transformation from both healthy bone marrow and myelodysplastic syndromes. (PMID:23100280)
  • miRNA-34b inhibits prostate cancer through demethylation, active chromatin modifications, and AKT pathways. (PMID:23147995)
  • Our results indicate that miR-34b/c enhances radiosensitivity (PMID:23155254)
  • the rs4938723 in the promoter region of pri-miR-34b/c was a protective factor for the development of colorectal cancer (PMID:23183747)
  • findings indicate that miR-34b acts as a tumor metastasis suppressor through negatively modulating Smad3, which may provide a potential therapeutic strategy for pancreatic cancer (PMID:23305226)
  • fi dings show that miR-34b may play an important role in non-small cell lung cancer progression; miR-34b downregulates Met, with subsequent changes of downstream p53 and Mdm2, and inversely p53 upregulates miR-34b in a feedback loop (PMID:23314612)
  • Polymorphisms of rs4938723 in the promoter region of pri-miR-34b is associated with nasopharyngeal carcinoma. (PMID:23504554)
  • Contributions of the polymorphisms and their multiplicative interactions with gender or HCC-related HBV mutations to HCC risk (PMID:23516510)
  • Downregulation of miR-34a, miR-34b and miR-34c induced an oncogenic phenotype in non-malignant mesothelial cells. (PMID:23525472)
  • Loss of the T allele in miR-34b/c T>C, and the miR-34b/c CC-TP53 Arg/Arg combination increases the risk of hepatocellular carcinoma in the Korean population. (PMID:23632240)
  • Studies suggest that rs4938723 is not associated with the risk of hepatocellular carcinoma (HCC). (PMID:23935875)
  • Our results suggest that the pri-miR-34b/c polymorphism rs4938723 is not associated with susceptibility to sporadic congenital heart disease in the Han Chinese population (PMID:24065649)
  • Epigenetic inactivation of miR-34b/c by DNA methylation has independent prognostic value in patients with early-stage lung adenocarcinoma. (PMID:24130071)
  • rs4938723 in the promoter region of pri-miR-34b/c and TP53 codon 72 were related to decreased risk of colorectal cancer and those metabolic diseases and genetic variants influence each other with regard to colorectal cancer susceptibility. (PMID:24337371)
  • A potentially functional polymorphism in the promoter region of miR-34b/c is associated with renal cell cancer risk in a Chinese population. (PMID:24503183)
  • miR-34b/c, in addition to DAPK1 and miR-34a might be inactivated by DNA hypermethylation, in in chronic lymphocytic leukemia. (PMID:24559316)
  • Abnormal methylation of miR-34a and miR-34b/c genes could play a role in colorectal cancer and potentially serve as biological markers (PMID:24573638)
  • miR-34b/c is a candidate tumor suppressor that is epigenetically silenced in chronic lymphocytic leukemia. (PMID:24686393)
  • DNA methylation may be involved in the inactivation of miR-34b in hepatocellular carcinoma. (PMID:24704024)
  • Methylation of DAPK1, miR-34a and -34b/c is tumour-specific, and associated with gene/miRNAs silencing in acute promyelocytic leukemia. (PMID:24811488)
  • Gene-environment interactions using MDR-pt program revealed that mir29a, mir34b, mir423 and Xpo5 modulated risk of disease (p < 0.002) which may be related to change in expression of these genes as observed by Real-Time PCR assays (PMID:24885463)

Cross-species orthologs

3 orthologs

OrganismSymbolGene ID
mus_musculusMir34bENSMUSG00000065492
drosophila_melanogastermir-34FBGN0262459
caenorhabditis_elegansWBGENE00003262

Paralogs (2): MIR34C (ENSG00000207562), MIR34A (ENSG00000284357)

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.