MIR17
gene geneOn this page
Also known as hsa-mir-17
Summary
MIR17 (microRNA 17, HGNC:31547) is a microRNA gene on chromosome 13q31.3.
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 406952 — 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
| Field | Value |
|---|---|
| HGNC ID | HGNC:31547 |
| Approved symbol | MIR17 |
| Name | microRNA 17 |
| Location | 13q31.3 |
| Locus type | RNA, micro |
| Status | Approved |
| Aliases | hsa-mir-17 |
| Ensembl gene | ENSG00000284536 |
| Ensembl biotype | miRNA |
| OMIM | 609416 |
| Entrez | 406952 |
| RNAcentral | URS000032AA22 — miRNA, 84 nt, 76 organism(s) |
Gene structure
Transcript identifiers
Ensembl transcripts: 1 — 1 miRNA
ENST00000385012
RefSeq mRNA: 0 — MANE Select: None
Canonical transcript exons
ENST00000385012 — 1 exons
| Exon | Start | End |
|---|---|---|
| ENSE00001500019 | 91350605 | 91350688 |
Expression profiles
Bgee: expression breadth tissue_specific, 8 present calls, max score 59.27.
Top tissues by expression
8 total, by Bgee expression score (0-100, higher = more expressed):
| Tissue | Anatomy ID | Expression score | Quality |
|---|---|---|---|
| renal glomerulus | UBERON:0000074 | 59.27 | silver quality |
| ovary | UBERON:0000992 | 55.75 | silver quality |
| left lobe of thyroid gland | UBERON:0001120 | 54.43 | gold quality |
| thyroid gland | UBERON:0002046 | 54.42 | gold quality |
| placenta | UBERON:0001987 | 51.47 | gold quality |
| islet of Langerhans | UBERON:0000006 | 51.16 | silver quality |
| testis | UBERON:0000473 | 35.12 | silver quality |
| left testis | UBERON:0004533 | 35.09 | gold quality |
Single-cell (SCXA)
Detected in 1 experiment(s), a significant marker in 0.
| Experiment | Marker? | Max mean expression |
|---|---|---|
| E-ANND-3 | no | 0.00 |
Regulation
Is transcription factor: no
Upstream regulators (CollecTRI, top): HIF1A, THRA
Literature-anchored findings (GeneRIF, showing 40)
- Enforced expression of the mir-17-92 cluster acted with c-myc expression to accelerate tumour development in a mouse B-cell lymphoma model (PMID:15944707)
- expression of E2F1 is negatively regulated by two miRNAs in the cluster, miR-17-5p and miR-20a (PMID:15944709)
- Data show that downregulation of AIB1 by Mir-17-5p resulted in decreased estrogen receptor-mediated, as well as estrogen receptor-independent, gene expression and decreased proliferation of breast cancer cells. (PMID:16940181)
- Altered miRNA expression may contribute to the pathophysiology of chronic myeloid leukemia. (PMID:17284533)
- Lymphocytes from transgenic mice with high expression of microRNA-17-92 show more proliferation and less activation-induced cell death, a mechanism which may contribute to lymphoma development in humans with amplifications of the miR-17-92 coding region. (PMID:18327259)
- a circuit involving c-myc, miR-17-92, and HIF-1 alpha may play a role in cancer cell proliferation under normoxia in a cellular context-dependent manner (PMID:18632605)
- PTPRO gene is co-regulated by both E2F1 and miR-17-92. (PMID:18644370)
- The combination of assays presented here supports a role for miR-17-92 polycistron and miR-21 in the maintenance of the malignant transformation of hepatocytes. (PMID:18688024)
- These studies identify a novel cyclin D1/miR-17/20 regulatory feedback loop through which cyclin D1 induces miR-17-5p/miR-20a. (PMID:18695042)
- findings show miR-17-5p acts specifically at the G1/S-phase cell cycle boundary, by targeting more than 20 genes involved in transition between these phases; miR-17-5p is able to act as both an oncogene & tumor suppressor in different cellular contexts (PMID:18700987)
- miRNA 17-5p, 20a and 126 are constitutively expressed in Ph(-) MPN megakaryopoiesis while low or absent miRNA 10a appeared to correlate with strong megakaryocytic HOXA1 protein expression (PMID:18773208)
- miR-17 and miR-20a govern the transition through G1 in normal diploid human cells. (PMID:18836483)
- CDKN1A/p21 appears to be an essential target of miR-17-92 during B-cell lymphomagenesis, which suggests the miR-17-92 polycistron has distinct targets in different B-cell lymphoma subtypes. (PMID:18941111)
- miR-17-92 plays a critical role in regulating the position of the off-on switch in E2F/Myc protein levels, and in determining the on levels of these proteins. (PMID:19066217)
- the deregulated miR expression pattern, miR-34a, miR-29 and miR-17-5p, in CLL patients with deleted and/or mutated p53 gene are closely associated to the biological subtypes of CLL (PMID:19158830)
- MiR-17-5p showed a significant higher expression level in the central nervous system compared with testicular and nodal diffuse large B-cell lymphomas (PMID:19287466)
- down regulation of miR-34a, miR-29 and miR-17-5p in aggressive CLL with TP53 abnormalities (PMID:19347736)
- Studies support the notion that miR-17 causes cellular defects through its repression of fibronectin expression. (PMID:19633662)
- Increased expression of miR-17-92 cluster during colorectal adenoma to adenocarcinoma progression is associated to DNA copy number gain of miR17-92 locus on 13q31 and c-myc expression. (PMID:19672269)
- microRNA-17 directly targets the 3’UTR of PKD2 and post-transcriptionally repress the expression of PKD2. (PMID:19821056)
- E-selectin and ICAM-1 are targets of TNF-induced miRNAs miR-31 and miR-17-3p, respectively. (PMID:19949084)
- A significant number of dysregulated proteins in clear cell renal cell carcinoma are potential miRNA targets. Also, many clear cell renal cell carcinoma dysregulated miRNAs are phylogenetically conserved. (PMID:20022054)
- identified four commonly regulated miRNAs, miR-17 down-regulated in all seven; miR-19b and miR-20a, down-regulated in six models; and miR-106a down-regulated in five models. (PMID:20089119)
- MiR-17-5p, which is involved in autoimmunity, was up-regulated in CD4(+) cells from MS patients. (PMID:20148420)
- findings suggest that the p38 MAPK pathway plays a crucial role in miR-17-5p-induced phosphorylation of HSP27 and, as a consequence, phosphorylated HSP27 enhances the migration of hepatocellular carcinoma cells (PMID:20209605)
- Results indicate that the detection of miR-106a and -17 in peripheral blood may be a novel tool for monitoring circulating tumor cells in patients with gastric cancers. (PMID:20349219)
- microRNA17/20 cluster is shown to govern cellular migration and invasion of nearby cells via heterotypic secreted signals. (PMID:20406904)
- miR-17-5p plays an important role in breast cancer cell invasion and migration by suppressing HBP1 and subsequent activation of Wnt/beta-catenin (PMID:20505989)
- VDUP1 expression was regulated by FOXO3A at the transcriptional level and by miR-17-5p at the post-transcriptional levels during the senescence process. (PMID:20656682)
- Findings suggest that miR-17-5p plays important roles in pancreatic carcinogenesis and cancer progression, and is associated with a poor prognosis in pancreatic cancer. (PMID:20703102)
- miR-17 and miR-20a were significantly under-expressed in multiple sclerosis (PMID:20711463)
- These results suggest c-Myc could further repress p21 expression at the post-transcriptional level through some, but not all, members of miR-17 family. (PMID:20878079)
- These findings are the first direct evidence that over-expression of miRNA-17-92 cluster significantly increases the radioresistance of human mantle cell lymphoma cells (PMID:21040528)
- Expression of miR-17-19b is inhibited in K562 cell line after 5-aza treatment. (PMID:21176349)
- miR-17* may suppress tumorigenicity of prostate cancer through inhibition of mitochondrial antioxidant enzymes (PMID:21203553)
- Mir-17, -20a, and -106b downregulate a common set of pro- and anti-proliferative target genes to impact cell cycle progression of human cord blood stem cells and increase intracellular activity of E2F transcription factors to govern G(1)/S transition. (PMID:21283765)
- This study suggested that Mir-17-3p-mediated repression of Olig2 mRNA plays a critical role during the patterning of ventral spinal progenitor domains by shifting the balance of cross-repressive interactions between Olig2 and Irx3 transcription factors. (PMID:21338882)
- The expression of miR-17-3p and miR-106a is regulated by TNFalpha and lipopolysaccharides in HeLa cells. (PMID:21370248)
- STAT3 mediates resistance to MEK inhibitor through microRNA miR-17 (PMID:21444672)
- Data show that miR-17/20 inhibition suppresses proliferation in cultured retinoblastoma cells. (PMID:21816922)
Cross-species orthologs
2 orthologs
| Organism | Symbol | Gene ID |
|---|---|---|
| mus_musculus | Mir17 | ENSMUSG00000065508 |
| rattus_norvegicus | Mir17 | ENSRNOG00000035657 |
Paralogs (4): MIR106B (ENSG00000208036), MIR20A (ENSG00000283762), MIR18A (ENSG00000283815), MIR20B (ENSG00000284043)
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.
Related Atlas pages
No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.