MIR17HG

Summary

MIR17HG (miR-17-92a-1 cluster host gene, HGNC:23564) is a long non-coding RNA gene on chromosome 13q31.3.

This gene is the host gene for the MIR17-92 cluster, a group of at least six microRNAs (miRNAs) that may be involved in cell survival, proliferation, differentiation, and angiogenesis. Amplification of this gene has been found in several lymphomas and solid tumors. Two non-protein coding transcript variants have been found for this host gene, but only the longest is a polycistronic transcript containing the MIR17-92 cluster.

Source: NCBI Gene 407975 — RefSeq curated summary.

At a glance

• Gene type: non-coding (lncRNA) — 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:23564
Approved symbol	MIR17HG
Name	miR-17-92a-1 cluster host gene
Location	13q31.3
Locus type	RNA, long non-coding
Status	Approved
Aliases	FLJ14178, MIRH1, MIHG1, NCRNA00048, miR-17-92, LINC00048
Ensembl gene	ENSG00000215417
Ensembl biotype	lncRNA
OMIM	609415
Entrez	407975
RNAcentral	URS0002A1475A — lncRNA, 1062 nt, 1 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 20 — 20 lncRNA

ENST00000400282, ENST00000581816, ENST00000582141, ENST00000659898, ENST00000664987, ENST00000710412, ENST00000710413, ENST00000710414, ENST00000710419, ENST00000710420, ENST00000710421, ENST00000710422, ENST00000710423, ENST00000710424, ENST00000710425, ENST00000710426, ENST00000718127, ENST00000833714, ENST00000833716, ENST00000833717

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000400282 — 4 exons

Exon	Start	End
ENSE00001542250	91350156	91350226
ENSE00001542252	91349698	91349770
ENSE00004250569	91347820	91347959
ENSE00004250571	91353933	91354823

Expression profiles

Bgee: expression breadth ubiquitous, 180 present calls, max score 88.40.

FANTOM5 (CAGE): breadth ubiquitous, TPM avg 17.2906 / max 962.7001, expressed in 1445 samples.

FANTOM5 promoters (3 alternative TSS)

Promoter ID	TPM avg	Samples expressed
135622	16.4904	1432
135623	0.5548	2
135624	0.2454	108

Top tissues by expression

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

Tissue	Anatomy ID	Expression score	Quality
primordial germ cell in gonad	CL:0000670 ∩ UBERON:0000991	88.40	gold quality
epithelial cell of pancreas	CL:0000083	84.58	silver quality
body of pancreas	UBERON:0001150	83.59	gold quality
adrenal tissue	UBERON:0018303	83.55	gold quality
male germ line stem cell (sensu Vertebrata) in testis	CL:0000089 ∩ UBERON:0000473	83.30	gold quality
buccal mucosa cell	CL:0002336	82.59	silver quality
mucosa of transverse colon	UBERON:0004991	79.59	gold quality
sural nerve	UBERON:0015488	79.55	gold quality
left uterine tube	UBERON:0001303	77.40	gold quality
vermiform appendix	UBERON:0001154	76.07	gold quality
calcaneal tendon	UBERON:0003701	75.56	gold quality
pancreas	UBERON:0001264	75.55	gold quality
bone marrow cell	CL:0002092	75.35	gold quality
colonic epithelium	UBERON:0000397	74.92	gold quality
spleen	UBERON:0002106	74.19	gold quality
body of stomach	UBERON:0001161	74.17	gold quality
right ovary	UBERON:0002118	74.16	gold quality
right lobe of thyroid gland	UBERON:0001119	73.90	gold quality
transverse colon	UBERON:0001157	73.81	gold quality
small intestine Peyer’s patch	UBERON:0003454	73.43	gold quality
oviduct epithelium	UBERON:0004804	73.28	gold quality
stomach	UBERON:0000945	73.00	gold quality
granulocyte	CL:0000094	72.90	gold quality
right lobe of liver	UBERON:0001114	72.78	gold quality
left ovary	UBERON:0002119	72.41	gold quality
omental fat pad	UBERON:0010414	72.25	gold quality
peritoneum	UBERON:0002358	72.17	gold quality
lymph node	UBERON:0000029	71.89	gold quality
gall bladder	UBERON:0002110	71.88	gold quality
left lobe of thyroid gland	UBERON:0001120	71.81	gold quality

Single-cell (SCXA)

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

Experiment	Marker?	Max mean expression
E-ANND-3	yes	5.95

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): EGR2, KDM5B, MBD2, MYC, MYCN, SPI1, TP53

Literature-anchored findings (GeneRIF, showing 40)

• miR-17-92 overexpression may serve as a fine-tuning influence to counterbalance the generation of DNA damage in RB-inactivated SCLC cells. (PMID:19597473)
• p53-mediated repression of miR-17-92 expression likely has an important function in hypoxia-induced apoptosis (PMID:19696742)
• The type-2-skewing tumor microenvironment induces the down-regulation of miR-17-92 expression in T cells, thereby diminishing the persistence of tumor-specific T cells and tumor control. (PMID:20167088)
• Auroroa kinase A induces miR-17-92 cluster through regulation of E2F1 transcription factor. (PMID:20300951)
• miR-17-92 and its target CTGF mediate effects of differentiation-promoting treatment on glioblastoma cells through multiple regulatory pathways. (PMID:20305691)
• the Myc-inducible miR-17-92 cluster miRNAs contribute to tumorigenesis and poor prognosis in multiple myeloma (PMID:21664042)
• study demonstrates that the MYCN-induced downregulation of Dickkopf-3 (DKK3) results from direct upregulation of miR-17-92 components effecting both DKK3 mRNA stability (PMID:21796614)
• We demonstrate that haploinsufficiency of miR-17 approximately 92 is responsible for skeletal and growth developmental abnormalities. (PMID:21892160)
• Upon macrophage differentiation PU.1 represses the miR-17-92 cluster promoter by an Egr-2/Jarid1b-mediated H3K4 demethylation mechanism whose deregulation may contribute to leukaemic states. (PMID:21897363)
• The network involving miR-17-92 exhibits high noise sensitivity due to a positive feedback loop and also maintains resistance to noise from a negative feedback loop. (PMID:22022595)
• members of the oncomir miR-17-92 cluster were upregulated, but themiR-125b/miR-99a/let-7c, miR-106b/miR-93/miR-25 and miR-212/miR-132 clusters are also coordinately regulated either by stromal cell contact alone or by CD154 (PMID:22024720)
• inhibition of miR-17 approximately 92 expression suppressed the PI3K/AKT pathway and inhibited tumor growth in a xenograft MCL mouse model (PMID:22116552)
• High miR-17-92 is associated with chronic lymphocytic leukemia. (PMID:22343732)
• Upreg’n of miR-17-92 cluster was seen in MYC-amplified AS compared to AS lacking MYC amplification and controls. Moreover, MYC-amplified ASs were associated with a significantly lower expression of THBS1 than AS without MYC amplification or controls. (PMID:22383169)
• Imbalanced miR-17-92 expression, also mediated by p53, directly transforms the hematopoietic compartment. (PMID:22451425)
• results reveal a temporal expression pattern of miR-17-92 by antigen-specific CD8(+) T cells during viral infection, the precise control of which is critical to the effector expansion and memory differentiation of CD8(+) T cells (PMID:22665768)
• Overexpression of miR-17-92 cluster accelerates cell proliferation. (PMID:22731656)
• Oncogenic microRNA 17-92 cluster is regulated by epithelial cell adhesion molecule and could be a potential therapeutic target in retinoblastoma. (PMID:22969266)
• MiR-17-92 cluster microRNAs regulate the mRNA expression of their target genes in a dose-dependent manner. (PMID:22995834)
• HDAC9 promotes angiogenesis and transcriptionally represses the endothelial cell miR-17-92 cluster. (PMID:23288173)
• c-Myc-regulated members of the miR-1792 and miR-106a363 clusters inhibit trophoblast differentiation by repressing GCM1 and CYP19A1. (PMID:23438603)
• c-Myc-mediated overexpression of miR-17-92 suppresses replication of hepatitis B virus in human hepatoma cells. (PMID:23532756)
• The combined detection of PTEN and miR-92 may provide critical clinical evidence for the early diagnosis and prognosis of hepatocellular carcinoma. (PMID:23546593)
• The structural complexity of mir-17-92 as a polycistronic miRNA oncogene, along with the complex mode of interactions among its components, constitutes the molecular basis for its unique functional complexity during normal and tumor development.[Review] (PMID:23550645)
• miR-17~92 miRNA cluster is up-regulated in transgenic mouse models of polycystic kidney disease. (PMID:23759744)
• the upregulation of miR-17-92 may play a role in the biology of adenoid cystic carcinoma (PMID:23825564)
• The miR-17-92 cluster was specifically required for the accumulation of activated Ag-specific Treg and for differentiation into IL-10-producing effector Treg. (PMID:23858035)
• miR-17~92 is a powerful cancer driver that coordinates the activation of multiple oncogenic pathways in lymphomagenesis (PMID:23921550)
• our data indicate that miR-17-92 modulates expression of critical T-box transcriptional regulators during midface development and is itself a target of Bmp-signaling and the craniofacial pioneer factor AP-2alpha (PMID:24068957)
• miR-17-92 cluster family is involved in medulloblastoma progression. (PMID:24145352)
• The Myc-miR-17-92-BCR axis, frequently affected by genomic rearrangements, constitutes a novel lymphomagenic feed-forward loop. (PMID:24169826)
• data demonstrate the role of miR-17~92 in regulation of apoptosis, and identify BCL2 as a therapeutic target of particular relevance in BCR-ABL-positive ALL. (PMID:24280866)
• High miR-17-92 expression is associated with pediatric high-grade glioma. (PMID:24305714)
• BMPR2 downregulation is mediated by miR-17-92. (PMID:24378993)
• Study describes a novel mechanism, involving c-Myc and miR-17-92, which integrates cell proliferation and apoptosis resistance. (PMID:24469837)
• The promoter of the miR-17-92 gene cluster is transactivated through the promoter binding of STAT3 while BIM expression is decreasesed during Toxoplasma gondii infection. (PMID:24583285)
• miR-17-92, particularly miR-19 as a key component, can induce proliferation of cardiomyocytes and help protect the heart from ischemic injury caused by Myocardial infarction. (PMID:24625819)
• Upregulation of microRNA-17-92 cluster associates with tumor progression in osteosarcoma. (PMID:24645838)
• the high sensitivity of leukemia cells to HQ17(3) may be associated with the reduction of topo IIalpha and c-Myc activities, as well as with the downregulation of the miR-17-92 cluster expression. (PMID:25140305)
• A novel IL-6/Stat3-miR-17-92 cluster-PTEN signaling axis is crucial for cholangiocarcinogenesis and tumor progression. (PMID:25239565)

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.