| mir-17 microRNA precursor family | |
|---|---|
 Predicted secondary structure and sequence conservation of mir-17 | |
| Identifiers | |
| Symbol | mir-17 |
| Rfam | RF00051 |
| miRBase | MI0000071 |
| miRBase family | MIPF0000001 |
| Other data | |
| RNA type | Gene; miRNA |
| Domain | Eukaryota |
| GO | GO:0035195 GO:0035068 |
| SO | SO:0001244 |
| PDB structures | PDBe |
The miR-17 microRNA precursor family are a group of related small non-coding RNA genes called microRNAs that regulate gene expression. The microRNA precursor miR-17 family, includes miR-20a/b, miR-93, and miR-106a/b. With the exception of miR-93, these microRNAs are produced from several microRNA gene clusters, which apparently arose from a series of ancient evolutionary genetic duplication events, and also include members of the miR-19, and miR-25 families. [1] These clusters are transcribed as long non-coding RNA transcripts that are processed to form ~70 nucleotide microRNA precursors, that are subsequently processed by the Dicer enzyme to give a ~22 nucleotide products. The mature microRNA products are thought to regulate expression levels of other genes through complementarity to the 3' UTR of specific target messenger RNA. [2] [3]
Contents
The paralogous miRNA gene clusters that give rise to miR-17 family microRNAs (miR-17~92, miR-106a~363, and miR-106b~25) have been implicated in a wide variety of malignancies and are sometimes referred to as oncomirs. [4] The oncogenic potential of these non-protein encoding genes was first identified in mouse viral tumorigenesis screens. [5] [6] [7] In humans, the activating mutations of miR-17~92 have been identified in non-Hodgkin's lymphoma, whereas the miRNA constituents of the clusters are overexpressed in a multiple cancer types. [8] [9] [10] High level expression of miR-17 family members induces cell proliferation, whereas deletion of the miR-17~92 cluster, in mice, is lethal and causes lung and lymphoid cell developmental defects. [11] In addition, in the nasopharyngeal carcinoma cell line, miR-20a and miR-20b has been shown to target the 3' UTR of vascular endothelial growth factor (VEGF) and repress the expression of VEGF, which is an important angiogenic factor. [12] [13] miR-20a detection in human faeces could be a non-invasive screening marker for colorectal cancer. [14]