MIR101-2

gene
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Also known as hsa-mir-101-2

Summary

MIR101-2 (microRNA 101-2, HGNC:31489) is a microRNA gene on chromosome 9p24.1.

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 406894 — 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:31489
Approved symbolMIR101-2
NamemicroRNA 101-2
Location9p24.1
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-101-2
Ensembl geneENSG00000199065
Ensembl biotypemiRNA
OMIM612512
Entrez406894
RNAcentralURS000075A0E6 — miRNA, 79 nt, 20 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000362195

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000362195 — 1 exons

ExonStartEnd
ENSE0000143695848502974850375

Expression profiles

Bgee: expression breadth broad, 27 present calls, max score 79.00.

Top tissues by expression

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

TissueAnatomy IDExpression scoreQuality
liverUBERON:000210779.00gold quality
monocyteCL:000057674.51gold quality
calcaneal tendonUBERON:000370172.99gold quality
bloodUBERON:000017871.34gold quality
lower esophagus muscularis layerUBERON:003583369.13gold quality
right atrium auricular regionUBERON:000663168.93gold quality
omental fat padUBERON:001041467.26gold quality
heart left ventricleUBERON:000208466.94gold quality
lungUBERON:000204866.11gold quality
ascending aortaUBERON:000149666.01gold quality
body of pancreasUBERON:000115065.37gold quality
upper lobe of left lungUBERON:000895265.28gold quality
stomachUBERON:000094564.83gold quality
skin of legUBERON:000151164.58gold quality
right frontal lobeUBERON:000281064.41gold quality
esophagus mucosaUBERON:000246964.33gold quality
skin of abdomenUBERON:000141664.11gold quality
left ovaryUBERON:000211963.66gold quality
small intestine Peyer’s patchUBERON:000345462.65gold quality
esophagogastric junction muscularis propriaUBERON:003584162.58gold quality
endocervixUBERON:000045862.21gold quality
left lobe of thyroid glandUBERON:000112059.70gold quality
spleenUBERON:000210657.96gold quality
body of uterusUBERON:000985356.37gold quality
metanephros cortexUBERON:001053355.94gold quality
left testisUBERON:000453340.05gold quality
right testisUBERON:000453437.11gold quality

Single-cell (SCXA)

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

ExperimentMarker?Max mean expression
E-ANND-3no0.99

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • study proposes that the genomic loss of miR-101 in cancer leads to overexpression of EZH2 and concomitant dysregulation of epigenetic pathways, resulting in cancer progression (PMID:19008416)
  • MicroRNA-101, which is aberrantly expressed in hepatocellular carcinoma, could repress the expression of the FOS oncogene. (PMID:19133651)
  • miR-101 and Ezh2 are key players in UVB-induced senescence of human diploid fibroblasts. (PMID:23557329)
  • MiR-101 downregulated the expression of CPEB1 through reversing the methylation status of the CPEB1 promoter. (PMID:23788032)
  • This study provides further data for the identification of a miRNA profile for glioblastoma and suggests that different-grade neoplasia could be characterized by different expression of specific miRNAs. (PMID:24412053)
  • Genetic variations in the flanking regions of miR-101-2 are associated with increased risk of breast cancer. (PMID:24475105)
  • Data showed that miR-101 was downregulated and its target EZH2 was upregulated in retinoblastoma tissues and ther expression is significantly associated with adverse clinicopathological and histopathological features. (PMID:24807198)
  • Downregulation of miR101 induced cell survival and cisplatin resistance through the upregulation of COX2 expression. (PMID:25109742)
  • miR-101 and miR-145 are specifically upregulated in adult lung and miR-101 directly acts on its cognate site in the CFTR-3’UTR in combination with an overlapping AU-rich element (PMID:25186262)
  • study of the role of miR-101 in glioblastoma stem cells (GSCs) and the potential mechanisms; overexpression of miR-101 inhibited proliferation, cell migration, invasion and promoted apoptosis of glioblastoma stem cells by directly targeting KLF6 (PMID:25230316)
  • The data thus suggest a novel AP-1/miR-101 regulatory circuitry, that is, AP-1 promotes the transcription of miR-101, whereas the expression of miR-101 reduces the level of ERK2 and c-Fos and thereby attenuates the AP-1 signaling. (PMID:25260594)
  • miR-101 regulates expression of EZH2 and contributes to progression of and cisplatin resistance in epithelial ovarian cancer. (PMID:25260883)
  • Suggest that decreased expression of miR-101 might promote metastasis of human esophageal squamous cell carcinoma by inducing accumulation of EZH2 protein. (PMID:25400732)
  • We for the first time proposed the role interleukin-1beta-mir-101-EZH2 axes in the particle-induced lung cancer (PMID:25428391)
  • EZH2 is both a transcriptional inhibitor and a target gene of miR-101 in HUVECs, and it contributes to some of the miR-101-induced defects of gestational diabetes-HUVECs. (PMID:25614281)
  • Data indicate that microRNA miR-101 negatively regulates vascular endothelial growth factor C (VEGF-C) protein expression post-transcriptionally. (PMID:25658842)
  • Define Snail and Slug/miR-101/EZH2 pathway as a novel regulatory axis of epithelial-mesenchymal transformation in tongue squamous cell carcinoma. (PMID:25762643)
  • Data show that sorafenib inhibited microRNA miR-101 expression and enhanced dual specificity phosphatase 1 (DUSP1) expression and lowered transforming growth factor beta I (TGF-beta) release in M2 macrophage, slowing macrophage-driven hepatocarcinoma. (PMID:26158762)
  • miR-101 is a potent tumor repressor that directly represses CDK8 expression (PMID:26286725)
  • MiR101 may suppress ICC9810 cell migration and invasion, at least partly via inhibition of VEGFC. (PMID:26299768)
  • STAT3 signaling downstream of CXCR7 is involved in miR-101 regulation of breast cancer cell behaviors. (PMID:26360780)
  • miR-101-2, miR-125b-2 and miR-451a act as potential tumor suppressors in primary gastric cancer. (PMID:26458815)
  • miR-27b, miR-101 and miR-128 inhibit angiogenesis by down-regulating VEGF-C expression in gastric cancers. (PMID:26460960)
  • the SNPs rs578481 and rs705509 locating in pri-miR-101-1 may play a role in genetic susceptibility to oral squamous cell carcinoma. (PMID:26490987)
  • COX-2 is a direct target of miR-101 in esophageal squamous cell carcinoma. (PMID:26556718)
  • Study demonstrated that miR-101 is a novel hypoxamir in breast cancer cells. Through directing cell apoptosis and cell cycle arrest, ectopic expression of miR-101 suppressed proliferation in breast cancer cells. Also, these results identified VHL as its direct target and demonstrated that miR-101 could increase HIF1alpha protein levels by repressing VHL in normoxia condition. (PMID:26841847)
  • Data suggest that microRNA miR-101 may inhibit MDA-MB-231 breast cancer cell proliferation and migration by repressing DNA methyltransferase 3a (DNMT3a) expression and up-regulating E-cadherin expression. (PMID:26927545)
  • our findings demonstrate a novel mechanism by which miR-101 attenuates the epithelial-mesenchymal transition and metastasis in gallbladder cancer cells (PMID:26968949)
  • We identified AMPK as a novel target of mir-101-3p in triple negative breast cancer (PMID:27145268)
  • Results show that mir-101 expression level is regulated by LncRNA XIST to modulates EZH2 in gastric cancer cells. (PMID:27620004)
  • miR-101-TGF-beta/SDF1-VE-cadherin/MMP2/LAMC2 networks regulate vascular mimicry in hepatocellular carcinoma. (PMID:27693460)
  • MicroRNA-101 reverses temozolomide resistance by inhibition of GSK3beta expression in glioblastoma cells. (PMID:27792996)
  • NEAT1 interacted with miR-101 modulates breast cancer growth by targeting EZH2 (PMID:28034643)
  • The study showed that miR-101 inhibited viability, induced apoptosis, pushed glucose metabolism flux from the pentose phosphate pathway into glycolysis in prostate cancer PC3 cell line by decreasing NADPH levels by throughly directly binding to 3’-UTR of TIGAR mRNA and repressing TIGAR expression. (PMID:28384067)
  • Restoration of miR-101 expression reversed chemoresistance of drug-resistant gastric cancer cells by inhibiting viability and enhancing apoptosis via targeting ANXA2. (PMID:28609840)
  • miR-101 expression and RISC binding is increased after cyclosporine treatment in kidney cells; targets and reduces expression of MAP3K1 in vitro (PMID:28925592)
  • PTBP1 enhances miR-101-guided AGO2 interaction with MCL1, thereby regulating miR-101-induced apoptosis and clonogenic cell survival inhibition in cells. (PMID:29748555)
  • miR-101 expression was significantly downregulated in cervical cancer tissues compared with that in normal tissues. Upregulating miR-101 expression in SiHa cells significantly facilitated cell apoptosis, inhibited proliferation, and induced cell cycle arrest, indicating that miR-101 acted as an anti-oncogene. (PMID:29953787)
  • In the 3rd trimester of physiological pregnancy, there is a 244% increase in expression of miR-101a and a decrease by 73% in expression of miR-328. Both of these changes can protect against fibrosis during volume overload occurring in physiological pregnancy (PMID:29962114)
  • Results show that miR-101 expression is reduced and associated with poor prognosis in p53 WT lung adenocarcinoma patients. miR-101 is upregulated in a p53-dependent manner after exposure of cells to Pol I inhibitors, and is involved in positive-feedback regulation of p53 via repression of EG5, resulting in induction of apoptosis. (PMID:30049386)

Cross-species orthologs

2 orthologs

OrganismSymbolGene ID
danio_reriomir101bENSDARG00000081347
rattus_norvegicusMir101-2ENSRNOG00000035532

Paralogs (1): MIR101-1 (ENSG00000199135)

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.