MIR106B

gene
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Also known as hsa-mir-106b

Summary

MIR106B (microRNA 106b, HGNC:31495) is a microRNA gene on chromosome 7q22.1.

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 406900 — 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:31495
Approved symbolMIR106B
NamemicroRNA 106b
Location7q22.1
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-106b
Ensembl geneENSG00000208036
Ensembl biotypemiRNA
OMIM612983
Entrez406900
RNAcentralURS00000600E6 — miRNA, 82 nt, 26 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385301

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385301 — 1 exons

ExonStartEnd
ENSE00001500307100093993100094074

Expression profiles

Bgee: expression breadth ubiquitous, 111 present calls, max score 96.92.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
sural nerveUBERON:001548896.92gold quality
granulocyteCL:000009492.00gold quality
bone marrowUBERON:000237186.40gold quality
vermiform appendixUBERON:000115483.70gold quality
calcaneal tendonUBERON:000370183.68gold quality
endometriumUBERON:000129582.69gold quality
skeletal muscle tissueUBERON:000113482.59gold quality
duodenumUBERON:000211482.49gold quality
placentaUBERON:000198779.38gold quality
bloodUBERON:000017879.12gold quality
lymph nodeUBERON:000002979.07gold quality
monocyteCL:000057677.96gold quality
adrenal tissueUBERON:001830377.82gold quality
right adrenal gland cortexUBERON:003582776.89gold quality
adrenal glandUBERON:000236976.51gold quality
muscle of legUBERON:000138376.34gold quality
left adrenal glandUBERON:000123476.30gold quality
left adrenal gland cortexUBERON:003582575.56gold quality
right adrenal glandUBERON:000123375.52gold quality
body of pancreasUBERON:000115075.15gold quality
body of stomachUBERON:000116174.95gold quality
stomachUBERON:000094574.78gold quality
small intestineUBERON:000210873.71gold quality
rectumUBERON:000105273.54gold quality
small intestine Peyer’s patchUBERON:000345473.35gold quality
gastrocnemiusUBERON:000138873.34gold quality
islet of LangerhansUBERON:000000673.33gold quality
spleenUBERON:000210673.27gold quality
apex of heartUBERON:000209873.26gold quality
gall bladderUBERON:000211073.10gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.29

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): E2F1

Literature-anchored findings (GeneRIF, showing 40)

  • p21 is a direct target of miR-106b. Its silencing plays a key role in miR-106b-induced cell-cycle phenotypes. miR-106b overrides a doxorubicin-induced DNA damage checkpoint. (PMID:18212054)
  • The miR-106b-25 cluster, including miR-106b, miR-93, and miR-25, is involved in E2F1 posttranscriptional regulation and may play a key role in the development of TGFbeta resistance in gastric cancer. (PMID:18328430)
  • Ectopic expression of miR106b in CLL cells demonstrated that Itch was a direct target of miR106b such that miR106b-induced decreases in Itch resulted in an accumulation of p73. (PMID:19096009)
  • Knock-down studies for the miR-106b-25 cluster, which includes miR-106b, miR-93 and miR-25, showed that the expression of the cluster is necessary for cell proliferation and for anchorage-independent growth. (PMID:19486339)
  • demonstrated that the intronic miR-106b~25 cluster cooperates with its host gene MCM7 in cellular transformation both in vitro and in vivo, so that the concomitant overexpression of MCM7 and the miRNA cluster triggers prostatic intraepithelial neoplasia (PMID:20388916)
  • Low miRNA-106b is associated with renal cell carcinoma. (PMID:20609231)
  • The deregulation of this miRNA cluster(Mir106b and Mir-25) may alter Treg cells activity in course of MS, by altering TGF-beta biological functions. (PMID:20637509)
  • Regulation of p21 gene expression by miR-106b was assessed in colon cancer tissues (PMID:21283757)
  • Mir-17, -20a, and -106b downregulate a common set of pro- and anti-proliferative target genes to impact cell cycle progression of human cord blood stem cells and increase intracellular activity of E2F transcription factors to govern G(1)/S transition. (PMID:21283765)
  • In Hodgkin’s lymphoma high miR-17/106b expression contributes to a dysfunctional p53 pathway and thereby also to the malignant phenotype. (PMID:21953646)
  • MiR-106b affects amyloidbeta metabolism by suppressing ATP-binding cassette sub-family A protein (ABCA)1 expression. (PMID:22119192)
  • the A to G base change of rs999885 may provide a protective effect against chronic HBV infection but an increased risk for HCC in HBV persistent carriers by altering the expression of the miR-106b-25 cluster (PMID:22393390)
  • miR-106b and miR-15b maybe mediated as robust regulators in apoptosis or angiogenesis following MI, respectively (PMID:22613985)
  • miR-20a and miR-106b (known to be closely related) were the two most robust upregulated miRNAs in pediatric brainstem gliomas compared to adult subtype (PMID:22825541)
  • showed that CASP7 is downregulated in primary prostate tumors and metastatic lesions across multiple data sets (PMID:22986525)
  • findings demonstrate that 15-LOX-1-mediated metabolism of DHA is required for it to upregulate SDC-1 and trigger the signaling pathway that elicits apoptosis in prostate cancer cells (PMID:23087084)
  • The mir106b cluster targets the expression of several genes that are directly disease- relevant and that provide a mechanism for cross-talk from the canonical RB pathway to PTEN and p21Cip1. (PMID:23255112)
  • Plasma miR-106b, miR-20a, and miR-221 have the potential as novel, non-invasive biomarkers for the early detection of gastric cancer (PMID:23307259)
  • progressive reduction in the plasma miR-106b level may reflect persistent and systemic changes even after the discontinuation of smoking in COPD patients. miR-106b may therefore play an important role in the pathogenesis of COPD. (PMID:23338559)
  • High expression of miR-106b is associated with glioma. (PMID:23377830)
  • miR-106b expression contributed to hepatocellular carcinoma metastasis by activating the epithelial-mesenchymal transition process promoting cell migration in vitro and metastasis in vivo. (PMID:23483935)
  • Data indicate that miR-106b-25 cluster (miR-106b, miR-93 and miR-25) targets the 3’UTR of the beta-TRCP2 transcript and increases the expression of Snail. (PMID:23611780)
  • miR-106b may promote cell cycling of gastric cancer cells through regulation of p21 and E2F5 target gene expression. (PMID:23803041)
  • study demonstrated that the combined detection of miR-106b and miR-181b has a considerable clinical value to diagnose patients with liver cirrhosis, especially those at early stage. (PMID:23805240)
  • miR-106b fine tunes ATG16L1 expression and autophagic activity in colon cancer. (PMID:23899543)
  • miR-106b can promote the proliferation and invasion of laryngeal carcinoma cells by directly targeting RUNX3, and RUXN3 knockdown can abolish this phenotype (PMID:23912048)
  • Downregulation of MIR106B is associated with invasive endometrial cancer. (PMID:24002805)
  • In human cell lines, MIR106B reduces levels of ATG16L1 and autophagy and prevents autophagy-dependent eradication of intracellular bacteria. This process also appears to be altered in colon tissues from patients with active Crohn’s disease. (PMID:24036151)
  • Hypoxia promotes neuronal and neuroendocrine differentiation of NC cells and PCa cells, respectively, by inducing the miR-106 b25 cluster. In turn, miR-106b25 comprised of miR-106b, miR-93 and miR-25, down-regulates the transcriptional repressor REST. (PMID:24135225)
  • Regulation function of miR-106b-5p and its targets impact glioma cell proliferation and apoptosis. (PMID:24166509)
  • Findings provide a novel drug resistance/EMT regulatory pathway controlled by the miR-106b~25 cluster by targeting a transcriptional activator of E-cadherin. (PMID:24270410)
  • a high level of miR-106b induced by TGF-beta determines the tumor-promoting effects of TGF-beta in breast cancer (PMID:24292682)
  • A genetic variant in the promoter region of miR-106b-25 cluster predicts clinical outcome of hepatitis B-related hepatocellular carcinoma in the Chinese. (PMID:24416400)
  • miR-106b is up-regulated in cancer associated fibroblasts compared with normal fibroblasts established from patients with gastric cancer, and the expression level of miR-106b is associated with poor prognosis (PMID:24842611)
  • miR-106b was found up-regulated in squamous cell carcinoma cancer tissues (PMID:24846066)
  • miR-106b-25/miR-17-92 clusters are polycistrons with oncogenic roles in hepatocellular carcinoma [review] (PMID:24876719)
  • These data suggested the upregulation involvement of miR-106b in medulloblastoma biology (PMID:25041637)
  • The miR-106b-25 cluster contributes to epithelial-to-mesenchymal transition in the kidney. (PMID:25094038)
  • data indicate that urinary cell-free miR-106b might provide new complementary tumor biomarkers for BCa (PMID:25168920)
  • Considering the relationship between three miRNAs and some clinical pathological factors (TNM stage), it was implied that miR-106b~25 could be the next potential tumor biomarker for diagnosis and predictive prognosis for gastric cancer patients. (PMID:25218271)

Cross-species orthologs

1 orthologs

OrganismSymbolGene ID
mus_musculusMir106bENSMUSG00000065514

Paralogs (4): MIR20A (ENSG00000283762), MIR18A (ENSG00000283815), MIR20B (ENSG00000284043), MIR17 (ENSG00000284536)

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.