MIR23A

gene
On this page

Also known as hsa-mir-23a

Summary

MIR23A (microRNA 23a, HGNC:31605) is a microRNA gene on chromosome 19p13.12.

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 407010 — 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:31605
Approved symbolMIR23A
NamemicroRNA 23a
Location19p13.12
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-23a
Ensembl geneENSG00000207980
Ensembl biotypemiRNA
OMIM607962
Entrez407010
RNAcentralURS00001CC864 — miRNA, 73 nt, 22 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000385245

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000385245 — 1 exons

ExonStartEnd
ENSE000015002511383658713836659

Expression profiles

Bgee: expression breadth broad, 23 present calls, max score 87.20.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
renal glomerulusUBERON:000007487.20gold quality
skeletal muscle tissueUBERON:000113484.27gold quality
muscle of legUBERON:000138376.83gold quality
gastrocnemiusUBERON:000138869.13gold quality
bloodUBERON:000017867.04gold quality
uterusUBERON:000099566.63gold quality
ovaryUBERON:000099265.37gold quality
thyroid glandUBERON:000204664.45gold quality
spleenUBERON:000210663.30gold quality
midbrainUBERON:000189160.41gold quality
substantia nigraUBERON:000203860.41gold quality
hypothalamusUBERON:000189858.38gold quality
placentaUBERON:000198758.31gold quality
muscle layer of sigmoid colonUBERON:003580557.52gold quality
pituitary glandUBERON:000000756.48gold quality
amygdalaUBERON:000187655.21gold quality
tibial arteryUBERON:000761054.99gold quality
islet of LangerhansUBERON:000000653.30gold quality
anterior cingulate cortexUBERON:000983552.33gold quality
prostate glandUBERON:000236748.11gold quality
skin of legUBERON:000151147.99gold quality
testisUBERON:000047339.79gold quality
left testisUBERON:000453339.75gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.00

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): MYC, NFATC3, NFKB, RELA

Literature-anchored findings (GeneRIF, showing 40)

  • miR-23a, 27a, and 24-2 upregulation induces caspase-dependent and -independent apoptosis in human embryonic kidney cells (PMID:19513126)
  • Studies indicate a role for Myc in stimulating glutamine catabolism, in part through the repression of miRNAs miR-23a and miR-23b. (PMID:20086171)
  • Data indicate that miR-23a promotes proliferative potential of human gastric adenocarcinoma cell line MGC803; miR-23a was consistently upregulated in human gastric adenocarcinoma tissues; target gene for miR-23a appears to be IL6R. (PMID:20698883)
  • Study show thatb miRNAs of miR-23a27a24-2 cluster in relation to various health and diseased conditions and highlight the cooperative effects of the miRNAs of this cluster. (PMID:20815877)
  • Taken together, this work underlines the role of ER stress in miR-23a27a24-2 cluster mediated apoptosis in HEK293T cells. (PMID:21593605)
  • The protection of RPE cells against oxidative damage is afforded by miR-23a through regulation of Fas, which may be a novel therapeutic target in retinal degenerative diseases. (PMID:21693609)
  • Areca nut extracts-induced miR-23a was correlated with a reduced FANCG expression and DSB repair, which might contribute to ANE-associated human malignancies. (PMID:21750350)
  • MiR-23a expression promotes colon carcinoma cell growth, invasion and metastasis through inhibition of the MTSS1 gene. (PMID:22455847)
  • p65 activation decreases miR-23a expression, which facilitates glutamine consumption allowing leukemic cells to use this alternative source of carbon and favoring their adaptation to the metabolic environment (PMID:22634383)
  • Mir-23a may play important roles in regulating apoptosis via decreasing XIAP expression in human ovarian granulosa cells. (PMID:22653319)
  • findings suggest that miR-23a regulates TGF-beta-induced epithelial-mesenchymal transition by targeting E-cadherin in lung cancer cells (PMID:22752005)
  • CREB promotes gliomagenesis and acts as a modulator of oncogenic mir-23a, which represses the tumor suppressor PTEN. (PMID:23019365)
  • The protection of HaCaT cells against ultraviolet B damage is afforded by miR-23a through regulation of topoisomerase-1\caspase7\serine-threonine kinase 4 protein. (PMID:23158364)
  • SON protein regulates GATA-2 through transcriptional control of the microRNA 23a27a24-2 cluster (PMID:23322776)
  • Data indicate that expression of miR-23a, miR-27a, miR-199b, miR-221, and miR-223 by qRT-PCR can diagnose leukemia of ambiguous lineage as myeloid or lymphoid. (PMID:23444217)
  • MiR23a and miR23b are potential biomarkers of ovarian endometriosis. (PMID:23450049)
  • Our study demonstrates for the first time the regulation of HOXB4 by miR-23a (PMID:23630040)
  • Data suggest epidermal growth factor induced the expression of c-MYC, which promoted the expression of mature miR-23a, miR-24-2, and miR-27a and subsequently decreased expression of Sprouty2 (SPRY2). (PMID:23649631)
  • The triple miRNA classifier of miR-193a-3p, miR-23a and miR-338-5p appears to be a potential blood biomarker for early detection of colorectal cancer (PMID:23758639)
  • this study reports the expressions of miR-23a in glioma tissues are up-regulated, and knockdown of endogenous miR-23a could inhibit the proliferation, invasion and migration of glioma cells (PMID:23865473)
  • A feedback loop consisting of microRNA 23a/27a and the beta-like globin suppressors KLF3 and SP1 regulates globin gene expression. (PMID:23918807)
  • miR-23a participates in the mechanism of the FasL-induced epithelial-mesenchymal transition process in gastrointestinal cancer. (PMID:23929433)
  • miR-23a and miR-125b, proved to be negatively associated with up-modulation of Blimp-1 occurring during IFN-alpha-driven dendritic cell differentiation. (PMID:23977359)
  • MiR-23a could directly bind to 3’untranslated region of TOP1 mRNA, and suppress the corresponding protein expression. (PMID:24103454)
  • miR-23a was upregulated in glioma. This overexpression promoted glioma cell invasion, probably by modulating MMP-14 via directly inhibiting the expression of HOXD10. (PMID:24305689)
  • High miR-23a expression is the independent prognostic factor of overall and recurrence-free survival rates, and miR-23a may be involved in the onset of hepatocarcinoma as an oncogene. (PMID:24417970)
  • High MIR23A expression is associated with malignant pleural mesothelioma. (PMID:24457242)
  • MicroRNA-23a mediates post-transcriptional regulation of CXCL12 in bone marrow stromal cells. (PMID:24584347)
  • miR-23a may have a role in diffuse large B-cell lymphoma and could be a potential diagnostic and/or prognostic marker (PMID:24659264)
  • Overexpression of miR-23a inhibited osteogenic differentiation of human bone marrow-derived mesenchymal stem cells at the cellular, mRNA, and protein levels. (PMID:24802236)
  • There is an interaction between miR-23a and IRS-1 in the modulation of the migration and invasion of NSCLC cells. (PMID:24898878)
  • Serum levels of miR-23a is significant decline in type 2 diabetes patients compared with pre-diabetes patient. (PMID:24981880)
  • the significance of miR-23a and PPP2R5E in the proliferation and apoptosis of gastric cancer cells (PMID:24997345)
  • The epigenetic silencing of miR-23a led to derepression of BCR/ABL expression, and consequently contributes to CML development and progression. (PMID:25213664)
  • miR-23a-3p causes cellular senescence by targeting hyaluronan synthase 2: possible implication for skin aging. (PMID:25264594)
  • Targeting miR-23a in CD8+ cytotoxic T lymphocytes prevents tumor-dependent immunosuppression. (PMID:25347474)
  • Cells overexpressing HSP70 had higher levels of miR-23a, maintained these levels after heat shock and accumulated lower levels of NOXA mRNA and protein. (PMID:25429623)
  • miR-23a may have an oncogenic function and enhance breast cancer progression. (PMID:25445205)
  • MiR-23a thus contributes to HSV-1 replication through the regulation of the IRF1-mediated antiviral signal pathway. (PMID:25461762)
  • miR-23a promotes cisplatin chemoresistance and protects cisplatin-induced apoptosis in TSCC cells through inducing Twist expression by a JNK-dependent mechanism (PMID:25501015)

Cross-species orthologs

4 orthologs

OrganismSymbolGene ID
danio_reriomir23a-1ENSDARG00000080548
danio_reriomir23a-2ENSDARG00000081477
danio_reriomir23a-3ENSDARG00000083526
mus_musculusMir23aENSMUSG00000065611

Paralogs (1): MIR23B (ENSG00000207563)

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.