MIR152

gene
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Also known as hsa-mir-152

Summary

MIR152 (microRNA 152, HGNC:31538) is a microRNA gene on chromosome 17q21.32.

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 406943 — 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:31538
Approved symbolMIR152
NamemicroRNA 152
Location17q21.32
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-152
Ensembl geneENSG00000207947
Ensembl biotypemiRNA
OMIM613788
Entrez406943
RNAcentralURS00006A0932 — miRNA, 87 nt, 7 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385212

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385212 — 1 exons

ExonStartEnd
ENSE000015002184803716148037247

Expression profiles

Bgee: expression breadth broad, 72 present calls, max score 84.59.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
skeletal muscle tissueUBERON:000113484.59gold quality
myometriumUBERON:000129682.16gold quality
muscle of legUBERON:000138381.49gold quality
Brodmann (1909) area 9UBERON:001354080.26gold quality
bloodUBERON:000017878.46gold quality
fundus of stomachUBERON:000116075.95gold quality
placentaUBERON:000198774.59gold quality
gastrocnemiusUBERON:000138874.49gold quality
monocyteCL:000057673.08gold quality
right lobe of thyroid glandUBERON:000111972.31gold quality
adult mammalian kidneyUBERON:000008271.79gold quality
heart left ventricleUBERON:000208471.33gold quality
stomachUBERON:000094569.70gold quality
endometriumUBERON:000129569.66gold quality
substantia nigraUBERON:000203869.40gold quality
midbrainUBERON:000189169.39gold quality
left coronary arteryUBERON:000162669.19gold quality
heartUBERON:000094868.99gold quality
amygdalaUBERON:000187668.79gold quality
transverse colonUBERON:000115768.30gold quality
muscle layer of sigmoid colonUBERON:003580568.12gold quality
esophagogastric junction muscularis propriaUBERON:003584167.87gold quality
lower esophagusUBERON:001347367.75gold quality
lower esophagus muscularis layerUBERON:003583367.74gold quality
uterusUBERON:000099567.62gold quality
right adrenal glandUBERON:000123367.41gold quality
tibial arteryUBERON:000761067.35gold quality
esophagus mucosaUBERON:000246967.08gold quality
thoracic aortaUBERON:000151567.00gold quality
ascending aortaUBERON:000149666.79gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.46

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): DNMT1, TFCP2

Literature-anchored findings (GeneRIF, showing 40)

  • Data show that expression of MIR152, MIR200B, and MIR338 is specifically modulated in neuroblastoma cell lines during differentiation and apoptosis. (PMID:20574809)
  • These findings support a tumor-suppressive role of miR-152 in the epigenetic aberration of HBV-related HCC and the potential development of miRNA-based targeted approaches for the treatment of HBV-related hepatocellular carcinoma. (PMID:20578129)
  • miR-152 is down-regulated and regulates DNMT1 in HBV (hepatitis B virus)-related HCC (hepatocellular carcinoma). (PMID:20578129)
  • Data show that hypermethylation at miR-148a and miR-152 was associated with microsatellite-unstable tumors and hypermethylation at miR-18b with sporadic (PMID:21327300)
  • these findings define a central role for miR-152 in endometrial cancer. (PMID:21868754)
  • miR-152 and miR-148a may be involved in the carcinogenesis of ovarian cancer through deregulation of cell proliferation. (PMID:21971665)
  • down-regulated mir-152 levels in preeclampsia patients (PMID:22095477)
  • reduced microRNA-152 can lose an inhibitory effect on DNA methyltransferase, which leads to hypermethylation of the ERalpha gene and a decrease of ERalpha level (PMID:22295098)
  • miR-148a and miR-152 down-regulate HLA-G expression by binding its 3’UTR (PMID:22438923)
  • Studied the effect of miRNA128 and miRNA152 on post-transcriptional regulation of CSF-1 mRNA in human ovarian cancer. ID’d a common target for both miR-128 and miR-152; also found that both miR-128 and miR-152 down-regulate CSF-1 mRNA. (PMID:22909061)
  • miR-148a and miR-152 act as tumor suppressors by targeting IGF-IR and IRS1, and that restoration of miR-148a/152 expression may provide a strategy for therapeutic application to treat BC patients. (PMID:22935141)
  • Downregulation of miR-152 is associated with neoplastic transformation. (PMID:23125218)
  • we have identified two miRNAs, miR-152 and miR-181a, upregulated in senescent human diploid fibroblasts (PMID:23238588)
  • Results indicate that miR-152 and miR-185 were involved in ovarian cancer cisplatin resistance in vitro and in vivo by targeting DNMT1 directly. (PMID:23318422)
  • Our findings suggest that miR-152 can act as a tumor suppressor that targets TGFalpha. miR-152 is a promising molecular target that inhibits prostate cancer cell migration and invasion. (PMID:23460133)
  • results demonstrate that plasma levels of selected miRNAs are potential biomarkers to differentiate localized PCa and mCRPC. (PMID:23574937)
  • Data show that TLR3 activation by poly I-C induces up-regulation of microRNA-29b, -29c, -148b, and -152 targeting DNA methyltransferases, leading to demethylation and reexpression of the oncosuppressor retinoic acid receptor beta (RARbeta). (PMID:23716670)
  • In conclusion, our studies in multiple bladder cancer cell lines and primary non-malignant urothelial cells suggest that hypermethylation of miR-152, miR-10a and miR-200b regulative DNA sequences might serve as epigenetic bladder cancer biomarkers. (PMID:23867826)
  • These findings provide important evidence that the reduced miR-152 expression by HCV core protein can indirectly lose an inhibitory effect on Wnt1, which might, at least partially lead to cell proliferation of liver cancer cells. (PMID:24416131)
  • miRs that are targeting DNMT-1 and modifying methylation status of tumor suppressor genes such as BNIP3 and SPARC can be applied in killing the pancreatic cancer cells and decreasing the tumorigenicity of these cells. (PMID:24448385)
  • Data indicate that miR-152 was inversely correlated with ADAM metallopeptidase domain 17 (ADAM17) expression in non-small cell lung cancer (NSCLC) tissues. (PMID:24780186)
  • miR-152 may be involved in the development of human atherosclerosis (PMID:24813629)
  • Underexpression of miR-152 is associated with hepatocellular carcinoma. (PMID:24998573)
  • There appeared to be a reciprocal regulatory relationship of miR-152/DNMT1 expression, as cells treated with siRNA DNMT1 caused miR-152 to be re-expressed in all prostate cancer cell lines. (PMID:25004396)
  • Low expression of miR-152 was associated with supraglottic laryngeal carcinoma. (PMID:25095980)
  • Decreased expression of miR-152 is associated with gastric cancer. (PMID:25119599)
  • miR-152 suppressed the proliferation and invasion of NSCLC cells by downregulating FGF2. (PMID:25190353)
  • miR-152 inhibited the cell proliferation, migration, invasion, and promoted apoptosis of glioblastoma stem cells by directly targeting KLF4. (PMID:25218589)
  • miR-152 controls both the expression of 14-3-3beta and HLA-G and exerts a dual role in tumor cells by both altering the immunogenicity and the tumorigenicity (PMID:25228695)
  • The haplotype of miR-152 distributed various in the positive lymphovascular invasion group compared to negative group. Polymorphisms of miR-148b rs11170877 and 12231393 and their haplotypes were predictive factors of susceptibility to gastri cancer. (PMID:25261463)
  • Our findings suggest that mir-152 inhibits cell proliferation and colony formation of CD133(+) hep3B cells by targeting KIT. (PMID:25311946)
  • Serum miR-148a, miR-148b, and miR-152 were significantly downregulated in NSCLC patients. The combination of four candidate miRNAs exhibited the highest predictive accuracy in non-small cell lung cancer screening compared (PMID:25501703)
  • miR-152 mediates the tumor-suppressive effects that knockdown of XIST exerts in glioblastoma stem cells. (PMID:25578780)
  • Disruption of PKM2/NF-kappaB/miR-148a/152 feedback loop can regulate cancer cell growth. (PMID:25703326)
  • MicroRNA-152 represses VEGF and TGFbeta1 expressions through post-transcriptional inhibition of prorenin receptor in human retinal endothelial cells. (PMID:25802486)
  • relative expression levels of miR-148/152 family (miR-148a, miR-148b, and miR-152) in serum of 36 non-small-cell lung carcinoma patients, 20 patients with benign pulmonary diseases, and 10 healthy individuals (PMID:25904302)
  • miR-152 and miR-17 serum levels were significantly elevated in patients with obesity (PMID:25912229)
  • HOTAIR inhibited miR-152 expression in gastric cancer cells under the interaction between the two.HOTAIR promotes HLA-G expression via inhibiting miR-152 in gastric cancer cells. (PMID:26187665)
  • miR-152 blocked DKK1 transcriptional activity by binding to the 3’UTR of DKK1 mRNA. (PMID:26400224)
  • Data show that the expression of human leucocyte antigen-G (HLA-G) was upregulated by hepatitis B virus (HBV) infection and microRNA miR-152. (PMID:26468017)

Cross-species orthologs

2 orthologs

OrganismSymbolGene ID
mus_musculusMir152ENSMUSG00000065515
rattus_norvegicusMir152ENSRNOG00000035539

Paralogs (2): MIR148A (ENSG00000199085), MIR148B (ENSG00000199122)

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.