MIR125B1

gene
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Also known as hsa-mir-125b-1

Summary

MIR125B1 (microRNA 125b-1, HGNC:31506) is a microRNA gene on chromosome 11q24.1.

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 406911 — 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:31506
Approved symbolMIR125B1
NamemicroRNA 125b-1
Location11q24.1
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-125b-1
Ensembl geneENSG00000207971
Ensembl biotypemiRNA
OMIM610104
Entrez406911
RNAcentralURS00002A66E1 — miRNA, 88 nt, 21 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385236

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385236 — 1 exons

ExonStartEnd
ENSE00001500242122099757122099844

Expression profiles

Bgee: expression breadth broad, 76 present calls, max score 92.30.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
adrenal tissueUBERON:001830392.30gold quality
kidneyUBERON:000211378.38gold quality
calcaneal tendonUBERON:000370177.91gold quality
muscle of legUBERON:000138377.78gold quality
left adrenal gland cortexUBERON:003582577.39gold quality
left uterine tubeUBERON:000130376.92gold quality
placentaUBERON:000198776.76gold quality
pancreasUBERON:000126475.48gold quality
monocyteCL:000057674.68gold quality
islet of LangerhansUBERON:000000674.54gold quality
stomachUBERON:000094573.77gold quality
gastrocnemiusUBERON:000138873.27gold quality
heart left ventricleUBERON:000208472.91gold quality
endometriumUBERON:000129572.66gold quality
heartUBERON:000094872.55gold quality
left adrenal glandUBERON:000123471.57gold quality
right adrenal gland cortexUBERON:003582771.53gold quality
descending thoracic aortaUBERON:000234571.06gold quality
lungUBERON:000204870.92gold quality
right ovaryUBERON:000211870.85gold quality
bloodUBERON:000017870.69gold quality
body of stomachUBERON:000116169.68gold quality
endocervixUBERON:000045869.63gold quality
left coronary arteryUBERON:000162669.59gold quality
ovaryUBERON:000099269.57gold quality
thoracic aortaUBERON:000151569.55gold quality
ascending aortaUBERON:000149669.37gold quality
right atrium auricular regionUBERON:000663169.36gold quality
intestineUBERON:000016069.33gold quality
left ovaryUBERON:000211969.07gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no1.17

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • miR-125b, a miRNA downregulated in both psoriasis and atopic eczema, was expressed mostly in organs that contain cells of ectodermal origin. It was expressed at a very low level in inflammatory cells in comparison to structural cells. (PMID:17622355)
  • GC-enriched hsa-miR-125b down-regulates the expression of IRF4 and PRDM1/BLIMP1, and memory B cell-enriched hsa-miR-223 down-regulates the expression of LMO2. (PMID:19047678)
  • The microRNA 125b1 can remarkably inhibit all-trans-retinoic acid-induced cell apoptosis. (PMID:19471102)
  • miRNA-125b up-regulation contributes to astrogliosis and to defects in the cell cycle that are characteristic of degenerating brain tissues. (PMID:20347935)
  • MicroRNA-125b confers the resistance of breast cancer cells to paclitaxel through suppression of pro-apoptotic Bcl-2 antagonist killer 1 (Bak1) expression (PMID:20460378)
  • study reports transcriptional activation of miR-125b-1 in the recurrent translocation, t(11;14)(q24;q32), involving IGH@ in B-cell precursor acute lymphoblastic leukemia extending the involvement of miR-125b-1 to lymphoid precursor transformation (PMID:20485370)
  • Decreased MicroRNA-125b is associated with bladder cancer. (PMID:20549700)
  • expression of miR-125b suppressed the tumor formation generated by injecting OC cells in nude mice. Our results suggest that aberrantly expressed miR-125b may contribute to OC development (PMID:20658525)
  • Data reveal that miR-125b regulates hematopoietic stem cell (HSC) survival and can promote lymphoid-fate decisions at the level of the HSC by preferentially expanding lymphoid-balanced and lymphoid-biased HSC. (PMID:21118986)
  • Compared to common acquired nevi, mir-125b was found to be significantly downregulated, and let-7c was significantly upregulated in atypic nevi. (PMID:21166724)
  • miR-125b could be an important prognostic indicator for colorectal cancer patients. (PMID:21399871)
  • Loss of miR-125b in psoriasis skin may contribute to hyperproliferation and aberrant differentiation of keratinocytes. (PMID:21412257)
  • CpG-rich region 1 upstream of miR-125b-1 was hypermethylated in the 2 breast cancer cell lines and invasive breast cancer tissues but not in normal adjacent tissues (NATs). (PMID:21444677)
  • Overexpression of miR-125b in HCC cells decreased PIGF expression, and altered the angiogenesis index. Furthermore, modulation of miR-125b also distorted expression of MMP-2 and -9, the mediators of enzymatic degradation of the extracellular matrix. (PMID:21703189)
  • Data show that Differentially expressed miRNAs including miR-99a, miR-100, miR-125b, miR-192, and miR-429 were detected in pancreatic cancer stem cells. (PMID:21785383)
  • miR-125b is involved in vascular calcification in vitro and in vivo. (PMID:21806957)
  • miR-125b plays an important role in the development of pediatric APL at least partially mediated by repressing BAK1 protein expression and could be a potential therapeutic target for treating pediatric APL failure. (PMID:21880154)
  • miR-125b, a target of CDX2, regulates cell differentiation through repression of the core binding factor in hematopoietic malignancies. (PMID:21903586)
  • Oxidative stress-mediated induction of miR-125b plays a specific role in the pathogenesis of Hailey-Hailey disease by regulating the expression of factors playing an important role in keratinocyte proliferation and differentiation. (PMID:21913998)
  • these results propose that miR-125b buffers and fine-tunes p53 network activity by regulating the dose of both proliferative and apoptotic regulators. (PMID:21935352)
  • Mycobacterium tuberculosis lipomannan blocks TNF biosynthesis by regulating macrophage MAPK-activated protein kinase 2 (MK2) and microRNA miR-125b. (PMID:21969554)
  • members of the oncomir miR-17-92 cluster were upregulated, but themiR-125b/miR-99a/let-7c, miR-106b/miR-93/miR-25 and miR-212/miR-132 clusters are also coordinately regulated either by stromal cell contact alone or by CD154 (PMID:22024720)
  • the expression of miR-125b is regulated by STAT3 at the level of transcription. STAT3 binds to the promoter region of miR-125b in vitro and serves as a transactivator. (PMID:22093834)
  • Among possible numerous targets of miR-125b, we showed ARID3B (AT-rich interactive domain 3B) to be a novel target with roles in cell motility in breast cancer cells. (PMID:22307404)
  • Aberrantly expressed miR-125b contributes to HEC1B cells invasion partly through directly down-regulating ERBB2 protein expression in endometrioid endometrial cancer. (PMID:22460089)
  • miR-125b can act as an oncogene in B-cell acute lymphoblastic leukemia by targeting ARID3a and mediating its repression. (PMID:22469780)
  • MicroRNAs miR-125a and miR-125b constitutively activate the NF-kappaB pathway by targeting the tumor necrosis factor alpha-induced protein 3 (TNFAIP3, A20). (PMID:22550173)
  • role of miR-125b in pro-metastasis by targeting STARD13 (PMID:22693547)
  • Down-regulation of miR-125b in chronic lymphocytic leukemias leads to metabolic adaptation of cells to a transformed state. (PMID:22723551)
  • miR-125b may promote apoptosis by suppressing the anti-apoptotic molecules of the Bcl-2 family and miR-125b downregulation may facilitate tumor development by giving cells the capability to survive under conditions of nutrient deprivation and chemotherapy (PMID:22824797)
  • Down-regulation of miR-125b is associated with breast cancer. (PMID:22898264)
  • a microRNA locus, miR-125b-1, in 11q24, may be involved in myelodysplastic syndrome (MDS) containing a t(2;11)(p21;q23-24) translocation [case report] (PMID:22944560)
  • The tumor-suppressive miR-125b served as a negative regulator of SUV39H1 (PMID:22991213)
  • The miR-125b negatively regulates MAD1 expression by binding to its 3’UTR. (PMID:23099851)
  • These findings reveal that ERBB2 and ERBB3 expression is regulated by ROS via miR-199a and miR-125b downregulation and DNA hypermethylation (PMID:23146892)
  • The expression of miR- 125b in HeLa cervical cancer cells decreased cell proliferation, induced apoptosis and down-regulated expression of PIK3CD. (PMID:23160634)
  • Down-regulation of miR-125b mainly in T cells may contribute to the pathogenesis of systemic lupus erythematosus by regulating ETS1 and STAT3 gene expression. (PMID:23305626)
  • Our results indicate that miR-125b plays an important role in regulating the expression of ADAMTS-4 in human chondrocytes (PMID:23406982)
  • miR-125b-1 causes mitogen-activated protein kinase pathway dysfunction through regulation of TACSTD2 expression. (PMID:23416980)
  • Data suggest that acute myeloid leukemia (AML) subtypes could be distinguished by by differentially expressed miRNAs including miR-126, -146a, -181a/b, -100, and miR-125b. (PMID:23418555)

Cross-species orthologs

4 orthologs

OrganismSymbolGene ID
danio_reriomir125b-2ENSDARG00000080032
danio_reriomir125b-1ENSDARG00000081350
mus_musculusMir125b-1ENSMUSG00000093354
rattus_norvegicusMir125b1ENSRNOG00000035550

Paralogs (7): MIR99B (ENSG00000207550), MIR99A (ENSG00000207638), MIR10B (ENSG00000207744), MIR125B2 (ENSG00000207863), MIR100 (ENSG00000207994), MIR125A (ENSG00000208008), MIR10A (ENSG00000284038)

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.

  • Disease cohort memberships (association, not causation — diseases whose associated-gene cohort lists this gene; a subset are also under Associated diseases): rheumatic heart disease