MIR629

gene
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Also known as hsa-mir-629

Summary

MIR629 (microRNA 629, HGNC:32885) is a microRNA gene on chromosome 15q23.

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 693214 — 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:32885
Approved symbolMIR629
NamemicroRNA 629
Location15q23
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-629
Ensembl geneENSG00000207965
Ensembl biotypemiRNA
Entrez693214
RNAcentralURS000075CA16 — miRNA, 97 nt, 3 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385230

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385230 — 1 exons

ExonStartEnd
ENSE000015002367007937270079468

Expression profiles

Bgee: expression breadth broad, 53 present calls, max score 78.54.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
bloodUBERON:000017878.54gold quality
bone marrowUBERON:000237178.07gold quality
monocyteCL:000057674.83gold quality
stomachUBERON:000094573.45gold quality
gastrocnemiusUBERON:000138873.31gold quality
body of stomachUBERON:000116173.20gold quality
liverUBERON:000210772.43gold quality
sural nerveUBERON:001548871.87gold quality
body of uterusUBERON:000985371.68gold quality
tibial arteryUBERON:000761070.60gold quality
transverse colonUBERON:000115768.35gold quality
caudate nucleusUBERON:000187368.35gold quality
thoracic aortaUBERON:000151568.24gold quality
vaginaUBERON:000099668.16gold quality
fundus of stomachUBERON:000116068.07gold quality
ascending aortaUBERON:000149667.99gold quality
left coronary arteryUBERON:000162667.75gold quality
esophagus mucosaUBERON:000246967.64gold quality
lower esophagus muscularis layerUBERON:003583367.37gold quality
heartUBERON:000094866.93gold quality
dorsolateral prefrontal cortexUBERON:000983466.88gold quality
tibial nerveUBERON:000132366.84gold quality
lungUBERON:000204866.80gold quality
colonUBERON:000115566.64gold quality
heart left ventricleUBERON:000208466.62gold quality
right frontal lobeUBERON:000281066.51gold quality
esophagogastric junction muscularis propriaUBERON:003584166.38gold quality
thoracic mammary glandUBERON:000520066.34gold quality
skin of legUBERON:000151166.26gold quality
left lobe of thyroid glandUBERON:000112066.12gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.22

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 23)

  • The hsa-miR-629 but not hsa-miR-499-5P had effect on modulation of NBS1 gene in vitro. (PMID:22114071)
  • miRNA-516a-3p, miRNA-629 and miRNA-525-5p are expressed in pediatric SLE patients with active disease (PMID:24687380)
  • Findings identify miR-629 as a potent regulator of the TGFb/Smad signaling pathway via TRIM33 in clear renal cell carcinoma. (PMID:25381221)
  • We have identified expression of miR-629-3p, miR-223-3p, and miR-142-3p as increased in patients with (severe) neutrophilic asthma and suggest that these miRNAs actively contribute to the disease pathogenesis by modulating proinflammatory and wound-repair pathways. (PMID:27155035)
  • The present study shows the independent predictive effect of miR-629-3p on lung metastasis in TNBC and reveals that the suppression of miR-629-3p attenuates pulmonary metastasis in experimental breast cancer by directly targeting LIFR, which is an inhibitor of multiple metastatic signaling pathways. (PMID:28629464)
  • Overexpression of miR-629 promoted the cell ability of migration and invasion and reduced ovarian cancer cell apoptosis. In addition, elevated cancer inhibition ability of TSPYL5 induced by the miR-629 inhibitor was significantly blocked by inhibition of TSPYL5. (PMID:28972400)
  • Authors found that miR-629 negatively regulated FOXO3 protein expression and decreased the activity of a luciferase reporter construct containing the FOXO3 3’-untranslated region. These results show that miR-629 regulates FOXO3 at the posttranscriptional level, resulting in enhanced cell proliferation and invasion of pancreatic carcinoma. (PMID:29072689)
  • The results presented here suggest that miR-629-5p functions as a tumor promoter by improving proliferation and migration and repressing apoptosis and 5-FU sensitivity in colorectal cancer progression by directly down-regulating CXXC4. (PMID:30042169)
  • Serum miR-629 was a significant predictor for overall survival and disease-free survival of pancreatic cancer patients. (PMID:30178840)
  • MiR-629 expression in nasopharyngeal carcinoma (NPC) tissues was significantly higher than that of adjacent normal samples. Cell migration and invasion abilities were remarkably increased by miR-629 mimics and decreased by inhibitor transfection. PDCD4 was verified as a direct target gene of miR-629 in NPC cells. Knockdown of PDCD4 in cells over-expressing miR-629 restored cell proliferation and metastasis. (PMID:30657562)
  • miR-629-5p activates beta-catenin signaling by downregulating SFRP2 and thus promotes the growth and metastasis of hepatocellular carcinoma (HCC); these data open up new prospects for HCC treatment (PMID:30954576)
  • MiR-629 regulates hypoxic pulmonary vascular remodelling by targeting FOXO3 and PERP. (PMID:31240850)
  • miR-629-3p-meditated downregulation of SFTPC may promote lung adenocarcinoma progression (PMID:31379200)
  • MiR-629-5p promotes the invasion of lung adenocarcinoma via increasing both tumor cell invasion and endothelial cell permeability. (PMID:32108166)
  • Circular RNA circNRIP1 promotes migration and invasion in cervical cancer by sponging miR-629-3p and regulating the PTP4A1/ERK1/2 pathway. (PMID:32457332)
  • MicroRNA-629 promotes the tumorigenesis of non-small-cell lung cancer by targeting FOXO1 and activating PI3K/AKT pathway. (PMID:32716350)
  • Upregulation of Serum miR-629 Predicts Poor Prognosis for Non-Small-Cell Lung Cancer. (PMID:33763157)
  • MicroRNA-629-5p promotes osteosarcoma proliferation and migration by targeting caveolin 1. (PMID:33886809)
  • Overexpression of Long Non-Coding RNA MIR22HG Represses Proliferation and Enhances Apoptosis via miR-629-5p/TET3 Axis in Osteosarcoma Cells. (PMID:34373436)
  • RNA-sequencing of human aortic valves identifies that miR-629-3p and TAGLN miRNA-mRNA pair involving in calcified aortic valve disease. (PMID:35776288)
  • Mir-629 Repressed LATS2 Expression and Promoted the Proliferation of Prostate Cancer Cells. (PMID:36990459)
  • Long Noncoding RNA MAGI2-AS3 Represses Cell Progression in Clear Cell Renal Cell Carcinoma by Modulating the miR-629-5p/PRDM16 Axis. (PMID:37602452)
  • Extracellular vesicle-mediated regulation of imatinib resistance in chronic myeloid leukemia via the miR-629-5p/SENP2/PI3K/AKT/mTOR axis. (PMID:39056503)

Cross-species orthologs

0 orthologs

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.