Target intelligence / Profile preview

Primary microRNA-17-92 cluster transcript (pri-miR-17-92)

Target
pri-miR-17-92
Molecular classification
Non-coding RNA, Primary microRNA transcript, Polycistronic microRNA cluster
01

Overview

The primary microRNA-17-92 cluster transcript (pri-miR-17-92), also known as MIR17HG or Oncomir-1, is a polycistronic non-coding RNA located on chromosome 13q31.3. It is processed into six mature microRNAs: miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1, which collectively regulate hundreds of target mRNAs involved in the E2F cell cycle pathway, PTEN/PI3K/AKT signaling, and the pro-apoptotic protein BIM. This cluster is frequently overexpressed in various malignancies, particularly B-cell lymphomas and solid tumors, where it acts as a potent oncogene by promoting cell survival and proliferation. Conversely, germline deletions of the cluster result in Feingold syndrome, characterized by skeletal abnormalities and microcephaly, highlighting its critical role in normal development. Therapeutic strategies primarily involve antisense oligonucleotides (ASOs) designed to sequester specific mature miRNAs within the cluster, such as RGLS4326 for polycystic kidney disease, or experimental small molecules targeting the tertiary structure of the primary transcript to inhibit its enzymatic processing into functional miRNAs.

Other names
MIR17HGOncomir-1C13orf25miR-17-92 cluster host geneMIR17-92 cluster
02

Mechanism of action

Antisense inhibition of mature microRNA activity; Small molecule binding to RNA secondary structures to prevent Drosha/Dicer processing; CRISPR-mediated gene editing.

03

Biological functions

Cell proliferationApoptosis inhibitionCell cycle regulationAngiogenesisHematopoiesisLung developmentImmune system modulation
04

Disease associations

Cancer (B-cell lymphoma, lung cancer, colorectal cancer, breast cancer)Autosomal dominant Feingold syndrome type 1Polycystic kidney diseaseCardiovascular diseaseAutoimmune disease
05

Safety considerations

Off-target suppression of essential developmental pathwaysRisk of Feingold syndrome-like phenotypes if over-inhibitedLiver toxicity associated with antisense oligonucleotide deliveryDisruption of normal hematopoiesis
06

Interacting drugs

RGLS4326 (Ladmirsen)

2 more in the full profile.

07

Biomarkers

MIR17HG amplification (13q31.3)Circulating miR-17 levelsmiR-19a expression levelsc-Myc expression levels (regulatory link)

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