MIR25

gene
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Also known as hsa-mir-25

Summary

MIR25 (microRNA 25, HGNC:31609) 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 407014 — 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:31609
Approved symbolMIR25
NamemicroRNA 25
Location7q22.1
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-25
Ensembl geneENSG00000207547
Ensembl biotypemiRNA
OMIM612150
Entrez407014
RNAcentralURS00000C85B2 — miRNA, 84 nt, 51 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000384816

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000384816 — 1 exons

ExonStartEnd
ENSE00001499823100093560100093643

Expression profiles

Bgee: expression breadth ubiquitous, 120 present calls, max score 95.85.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
granulocyteCL:000009495.85gold quality
endometriumUBERON:000129595.16gold quality
bone marrowUBERON:000237194.70gold quality
vermiform appendixUBERON:000115492.98gold quality
mucosa of transverse colonUBERON:000499192.43gold quality
duodenumUBERON:000211490.84gold quality
spleenUBERON:000210690.36gold quality
skeletal muscle tissueUBERON:000113489.86gold quality
right uterine tubeUBERON:000130289.81gold quality
small intestineUBERON:000210889.16gold quality
small intestine Peyer’s patchUBERON:000345489.02gold quality
body of stomachUBERON:000116187.74gold quality
tonsilUBERON:000237287.49gold quality
stomachUBERON:000094587.26gold quality
primordial germ cell in gonadCL:0000670 ∩ UBERON:000099186.91gold quality
transverse colonUBERON:000115786.68gold quality
adrenal tissueUBERON:001830386.53gold quality
placentaUBERON:000198786.51gold quality
right hemisphere of cerebellumUBERON:001489086.06gold quality
right adrenal glandUBERON:000123385.81gold quality
body of pancreasUBERON:000115085.66gold quality
right adrenal gland cortexUBERON:003582785.62gold quality
intestineUBERON:000016085.15gold quality
adrenal glandUBERON:000236984.62gold quality
left adrenal gland cortexUBERON:003582584.57gold quality
cerebellar hemisphereUBERON:000224584.54gold quality
left adrenal glandUBERON:000123484.36gold quality
uterusUBERON:000099584.33gold quality
fundus of stomachUBERON:000116083.80gold quality
colonUBERON:000115583.73gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.82

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • Suggest that the miR-106b-25 cluster is involved in E2F1 posttranscriptional regulation and may play a key role in the development of TGFbeta resistance in gastric cancer. (PMID:18328430)
  • 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)
  • inhibition of miR-25 in cytokine-stimulated ASM cells up-regulates KLF4 expression via a post-transcriptional mechanism. (PMID:19541842)
  • 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)
  • 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)
  • In addition to miR-125b and miR-504, the human TP53 gene is negatively regulated by two more miRNAs: miR-25 and miR-30d. (PMID:20935678)
  • miR-25 target DR4 provides a mechanism by which miR-25 contributes to evasion of TRAIL-induced cholangiocarcinoma apoptosis (PMID:21953056)
  • miR-25 directly regulates apoptosis by targeting Bim in ovarian cancer. (PMID:22076535)
  • results define miR-25 and -32 as positive regulators of p53, underscoring their role in tumorigenesis in glioblastoma (PMID:22431589)
  • These results, for the first time, demonstrate that miR-25 promotes esophageal squamous cell carcinoma cell migration and invasion by suppressing CDH1 expression. (PMID:22450326)
  • miR-25 associates to residual beta-cell function and glycaemic control during disease progression (PMID:22829805)
  • MIR25 targets the mitochondrial calcium uniporter (MCU) and its overexpression in HeLa cells drastically reduces MCU levels and mitochondrial Ca(2+) uptake, while leaving other mitochondrial parameters and cytosolic Ca(2+) signals unaffected. (PMID:23246404)
  • MiR-25 may function as a tumor suppressor by targeting Smad7 in colon cancer. (PMID:23435373)
  • 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)
  • Data indicate that miR-17-92 families miR-19b, miR-20a, miR-25 and miR-92a might implicate in apoptosis induction in the some of the cells and conditions. (PMID:23681423)
  • MiR-25-3p inhibited the proliferation of tongue squamous cell carcinoma cells and regulated cell cycle-related protein expression. (PMID:23827155)
  • our work suggests that miR-25-mediated down-regulation of DSC2 promotes esophageal squamous cell carcinoma cell aggressiveness through redistributing adherens junctions and activating beta-catenin signalling (PMID:23836524)
  • miR-25 might promote gastric cancer cell growth and motility partially by targeting RECK. (PMID:24078004)
  • miR-25 expression is increased in colorectal cancer and may have a role in tumor progression (PMID:24293092)
  • miR-25, miR-223, and miR-375 were abnormally expressed in ESCC tissues and sera. Serum miR-223 and miR-375 are potential prognostic biomarkers for ESCC. (PMID:24390317)
  • Our data suggests that the overexpression of miR-25 in hepatocellular carcinoma tissues is of predictive value on poor prognosis (PMID:24593846)
  • Tissue miR-25 expression may be associated with tumor progression and have prognostic implications in female lung Adenocarcinoma patients. (PMID:24606441)
  • Genetic variation in MIR25 is associated with gastric cancer. (PMID:24643999)
  • increased expression of endogenous miR-25 contributes to declining cardiac function during heart failure and suggest that it might be targeted therapeutically to restore function (PMID:24670661)
  • The increased expression of miR-25 is closely related to poor prognosis of epithelial ovarian cancer (PMID:24696291)
  • The protein expression of p27, a cellcycle inhibitor, is negatively regulated by miR25. (PMID:24859599)
  • The levels of expression of 25 miRNA remained high and ten of these miRNA showed different expression from that at day 0. (PMID:24960647)
  • miR-25 promotes GC progression by directly downregulating TOB1 expression, and may be a noninvasive biomarker for the prognosis of GC patients. (PMID:25043310)
  • abnormal upregulation of ANGPTL2 in colorectal cancer is associated with miR-25 downregulation (PMID:25174582)
  • miR-25 negatively regulated LATS2 expression and promoted OC cell growth and motility. (PMID:25179841)
  • The expression of the miR-25/93/106b family may be regulated through mechanisms distinct from its host gene, MCM7 (PMID:25243570)
  • Logistic regression analysis demonstrated that miR-16 and miR-25 were independent factors for intracranial aneurysm occurrence. (PMID:25249297)
  • MiR-25, by targeting CDC42, is an important regulator in NSCLC. (PMID:25432132)
  • miR-25 reduced both wild-type and polyQ-expanded mutant ataxin-3 protein levels by interacting with the 3’UTR of ATXN3 mRNA (PMID:25451224)
  • Our study shows miR-25 is overexpressed in small cell lung cancer and acting as oncogenic regulator by regulating cyclin E2. (PMID:25550809)
  • MiR-25 promotes cell proliferation by targeting RECK in human cervical carcinoma. (PMID:25575057)
  • By applying loss-and-gain function analysis in NSCLC cell lines, we demonstrated that miR-25-BTG2 axis could directly regulated BTG2 expression and affect radiotherapy sensitivity of NSCLC cells. (PMID:25576360)
  • High MIRN25 expression is associated with esophageal adenocarcinoma. (PMID:25784377)
  • miR-25/miR-107-LATS2 axis might play an important role in proliferation and invasion of the gastric cancer cells (PMID:25824045)
  • our observations suggest that miR-25 is a key regulator of invasiveness in human prostate cancer through its direct interactions with av- and a6-integrin expression (PMID:25858144)

Cross-species orthologs

2 orthologs

OrganismSymbolGene ID
danio_reriomir25ENSDARG00000101889
mus_musculusMir25ENSMUSG00000065394

Paralogs (2): MIR92A1 (ENSG00000283705), MIR92A2 (ENSG00000284538)

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.