MIR103B1

gene
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Also known as hsa-mir-103-1-ashsa-mir-103b-1

Summary

MIR103B1 (microRNA 103b-1, HGNC:35384) is a microRNA gene on chromosome 5q34.

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 100302238 — 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:35384
Approved symbolMIR103B1
NamemicroRNA 103b-1
Location5q34
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-103-1-as, hsa-mir-103b-1
Ensembl geneENSG00000283612
Ensembl biotypemiRNA
Entrez100302238
RNAcentralURS000075ED36 — ncRNA, 62 nt, 4 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000636572

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000636572 — 1 exons

ExonStartEnd
ENSE00003796464168560904168560965

Expression profiles

Bgee: expression breadth tissue_specific, 3 present calls, max score 87.43.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
liverUBERON:000210787.43gold quality
cerebellar hemisphereUBERON:000224559.91gold quality
left testisUBERON:000453347.02gold 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

Literature-anchored findings (GeneRIF, showing 5)

  • MiR-103 significantly promotes cancer cell proliferation, invasion and metastasis, and, thus, could be an important mediator in the pathogenesis of colorectal cancer Through regulation of colorectal cancer cell DICER and PTEN expression. (PMID:24828205)
  • miR-103 is involved in insulin resistance and NAFLD, and may be a molecular link between insulin resistance and NAFLD (PMID:25593466)
  • Study results demonstrated that serum miR-103 was overexpressed in colorectal cancer (CRC) subjects, could differentiate CRC cases from controls with relatively high accuracy, and significantly correlated with worse clinical factors, as well as poorer recurrence-free survival or overall survival. Taken together, serum miR-103 might be a promising biomarker for diagnosis and prognosis of CRC. (PMID:30058684)
  • Clinical data indicates that a high expression of miR103 is associated with the progression of hepatocellular carcinoma (HCC). Further results suggest that miR103 promotes HCC metastasis and EMT by directly inhibiting LATS2. (PMID:30272278)
  • miR-103a and miR-103b had high complementarity and conservation, modulated reporter gene expression through seed sequences in the 3’UTRs of CAV-1 and SFRP4 mRNA, and negatively regulated their mRNA and protein levels (PMID:31583475)

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.