MIR339

gene
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Also known as hsa-mir-339

Summary

MIR339 (microRNA 339, HGNC:31776) is a microRNA gene on chromosome 7p22.3.

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 442907 — 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:31776
Approved symbolMIR339
NamemicroRNA 339
Location7p22.3
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-339
Ensembl geneENSG00000199023
Ensembl biotypemiRNA
OMIM615977
Entrez442907
RNAcentralURS000075B703 — miRNA, 94 nt, 3 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000362153

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000362153 — 1 exons

ExonStartEnd
ENSE0000143691610229331023026

Expression profiles

Bgee: expression breadth ubiquitous, 102 present calls, max score 85.08.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
right hemisphere of cerebellumUBERON:001489085.08gold quality
adenohypophysisUBERON:000219684.88gold quality
right coronary arteryUBERON:000162584.67gold quality
cerebellar hemisphereUBERON:000224583.69gold quality
bone marrowUBERON:000237183.12gold quality
pituitary glandUBERON:000000782.57gold quality
olfactory segment of nasal mucosaUBERON:000538682.17gold quality
prefrontal cortexUBERON:000045181.17gold quality
brainUBERON:000095578.04gold quality
right frontal lobeUBERON:000281077.88gold quality
frontal cortexUBERON:000187077.84gold quality
sural nerveUBERON:001548877.82gold quality
anterior cingulate cortexUBERON:000983577.73gold quality
amygdalaUBERON:000187677.59gold quality
monocyteCL:000057677.48gold quality
tibial arteryUBERON:000761077.45gold quality
popliteal arteryUBERON:000225077.41gold quality
cerebral cortexUBERON:000095677.27gold quality
dorsolateral prefrontal cortexUBERON:000983477.15gold quality
Brodmann (1909) area 9UBERON:001354077.07gold quality
putamenUBERON:000187476.71gold quality
left uterine tubeUBERON:000130376.50gold quality
Ammon’s hornUBERON:000195476.33gold quality
leukocyteCL:000073876.28gold quality
bloodUBERON:000017876.20gold quality
lymph nodeUBERON:000002976.03gold quality
muscle of legUBERON:000138375.95gold quality
thoracic aortaUBERON:000151575.92gold quality
ascending aortaUBERON:000149675.88gold quality
left coronary arteryUBERON:000162675.73gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.43

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 38)

  • Results show that Dicer is responsible for the generation of the mature miR-222 and -339, which suppress ICAM-1 expression on tumor cells. (PMID:19520829)
  • MiR-339-5p inhibits breast cancer cell migration and invasion (PMID:20932331)
  • miR-339-5p regulates BACE1 expression in human brain cells. (PMID:24352696)
  • Author show that a negative correlation between miR-339-5p and MDM2 expression exists in human cancer, implying that the interaction is important for cancer development. (PMID:24882579)
  • The results highlighted an important role of microRNA-339-5p in suppression of colorectal tumorigenesis, and also revealed that regulating the p53 function is an important mechanism for microRNA-339-5p in tumor suppression. (PMID:25193859)
  • Our results indicated that miR-339-5p may serve as a tumor suppressor and play important role in inhibiting tumor invasion. Our work implicates that miR-339-5p may serve as a prognostic marker and molecular therapeutic target in hepatocellular carcinoma (PMID:26186881)
  • Data indicate RNA binding protein NOVA1 as a target of microRNA miR-339. (PMID:26391641)
  • miR-339-5p inhibits migration and invasion in ovarian cancer by targeting NACC1 and BCL6. miR-339-5p may be a biomarker of metastasis in ovarian cancer; NACC1 had a predictive value for ovarian cancer progression (PMID:26553360)
  • Transduction of miR-339 and miR-766 expressing viruses into colon cancer cell lines (SW480 and HCT116) decreased DNMT3B expression (1.5, 3-fold) and (3, 4-fold), respectively. In addition, DNA methylation of some tumor suppressor genes decreased. (PMID:27668319)
  • miR-339-5p downregulation contributes to Taxol resistance in small-cell lung cancer by targeting FUT1. (PMID:28940895)
  • Plasma miR-339-5p or miR-21 could serve as a potential biomarker for diagnosis of lung adenocarcinoma (PMID:29103767)
  • MiR-339 targets the 3’-untranslated region of Skp2 mRNA to depress the proliferation of lung cancer cells. (PMID:29377618)
  • miR-339-5p promotes proliferation and survival of Stem Cell Leukemia/Lymphoma Syndrome cells through downregulation of the BCL2L11 and BAX pro-apoptotic genes (PMID:29735550)
  • miR-339-5p was downregulated in AML samples and cell lines. miR-339-5p overexpression inhibited cell proliferation, induced cell cycle arrest and increased apoptosis of AML by directly targeting SOX4. (PMID:30320397)
  • Data revealed a significant upregulation of miR-339 in patients affected with senile cardiac amyloidosis compared to controls. miR-339 is a potential candidate as biomarker for senile cardiac amyloidosis. (PMID:30332417)
  • Overexpression of miR-339-5p enhanced radiosensitivity of A549 and H460 cells by inhibiting cell viability, increasing apoptosis, inducing cell cycle arrest, and suppressing cell proliferation. Further exploration validated that miR-339-5p can target phosphatases of regenerating liver-1 (PRL-1) in lung cancer cells. (PMID:30462625)
  • Over-expression of MAFG-AS1 significantly decreased the level of miR-339-5p in NSCLC cell. Moreover, the matrix metalloproteinase 15 (MMP15) was identified to be a target of miR-339-5p. (PMID:30599080)
  • MiR-339-5p is a target of MALAT1 in breast cancer tissues.MiR-339-5p targeted and regulated BLCAP mRNA expression. (PMID:30683807)
  • Exosome-derived miR-339-5p mediates radiosensitivity through downregulation of Cdc25A, and predicts pathological response to preoperative radiotherapy in locally advanced Esophageal squamous cell carcinoma, suggesting it could be a promising non-invasive biomarker for facilitating personalized treatments. (PMID:30858545)
  • LncRNA ANRIL regulates cell proliferation and migration via sponging miR-339-5p and regulating FRS2 expression in atherosclerosis. (PMID:32141564)
  • LINC00467 knockdown repressed cell proliferation but stimulated cell apoptosis in glioblastoma via miR-339-3p/IP6K2 axis. (PMID:32176627)
  • MiRNA-339-5p suppresses the malignant development of gastric cancer via targeting ALKBH1. (PMID:32380054)
  • lncRNA SNHG11 promotes the development of colorectal cancer by mediating miR-339-3p/SHOX2. (PMID:32683847)
  • MiR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses and apoptosis by targeting TLR4. (PMID:32757169)
  • Serum miR-339-3p as a potential diagnostic marker for non-small cell lung cancer. (PMID:32944397)
  • Cross-talk between the ER pathway and the lncRNA MAFG-AS1/miR-339-5p/ CDK2 axis promotes progression of ER+ breast cancer and confers tamoxifen resistance. (PMID:33098638)
  • MiR-339 is a potential biomarker of coronary heart disease to aggravate oxidative stress through Nrf2/FOXO3 targeting Sirt2. (PMID:33849089)
  • Cardiomyocyte-produced miR-339-5p mediates pathology in Duchenne muscular dystrophy cardiomyopathy. (PMID:34270708)
  • Reactivation of tumour suppressor in breast cancer by enhancer switching through NamiRNA network. (PMID:34329471)
  • CircDOCK1 promotes the tumorigenesis and cisplatin resistance of osteogenic sarcoma via the miR-339-3p/IGF1R axis. (PMID:34876132)
  • [Hsa_circ_0005221 promotes prostate cancer progression through the miR-339-5p/STAT5a pathway]. (PMID:34914211)
  • CircRNA_0001795 sponges miRNA-339-5p to regulate yes-associated protein 1 expression and attenuate osteoporosis progression. (PMID:35040370)
  • The role of miRNA-339-5p in the function of vascular endothelial progenitor cells in patients with PCOS. (PMID:35151575)
  • Inhibitory Effect of miR-339-5p on Glioma through PTP4A1/HMGB1 Pathway. (PMID:35872698)
  • miR-339-3p inhibits cell growth and epithelial-mesenchymal transition in nasopharyngeal carcinoma by modulating the KAT6A/TRIM24 axis. (PMID:35976474)
  • Association of circulatory Klotho levels and its expression with miRNA- 339 in patients with schizophrenia. (PMID:36842554)
  • KCNQ1OT1 promotes retinoblastoma progression by targeting miR-339-3p that suppresses KIF23. (PMID:37198502)
  • hsa_circ_0020378 regulating miR-339-3p/COL1A1 promotes osteosarcoma progression. (PMID:37978903)

Cross-species orthologs

2 orthologs

OrganismSymbolGene ID
mus_musculusMir339ENSMUSG00000065593
rattus_norvegicusMir339ENSRNOG00000035479

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.