Mir-19 microRNA precursor family

Last updated
mir-19 microRNA precursor family
RF00245.jpg
Predicted secondary structure and sequence conservation of mir-19
Identifiers
Symbolmir-19
Rfam RF00245
miRBase MI0000073
miRBase family MIPF0000011
Other data
RNA type Gene; miRNA
Domain(s) Eukaryota
GO GO:0035195 GO:0035068
SO SO:0001244
PDB structures PDBe

There are 89 known sequences today in the microRNA 19 (miR-19) family but it will change quickly. They are found in a large number of vertebrate species. The miR-19 microRNA precursor is a small non-coding RNA molecule that regulates gene expression. Within the human and mouse genome there are three copies of this microRNA that are processed from multiple predicted precursor hairpins: [1] [2] [3]

Contents

* miR-19a on chromosome 14 (MI0000688)
* miR-19b-1 on chromosome 14 (MI0000718)
* miR-19b-2 on chromosome X (MI0000546)
* miR-19a on chromosome 13 (MI0000073)
* miR-19b-1 on chromosome 13 (MI0000074)
* miR-19b-2 on chromosome X (MI000075).

MiR-19 has now been predicted or experimentally confirmed (MIPF0000011). In this case the mature sequence is excised from the 3' arm of the hairpin precursor.

Origins

MicroRNA are ubiquitous in higher eukaryotes, and show varying patterns of expression in specific cell types. [4] MiR-19 has been identified in a diverse range of vertebrate animals including green anole (Anolis carolinensis), [5] primates (gorilla, human, ...), [6] [7] cattle (Bos taurus), [8] dog (Canis familiaris), [9] Chinese hamster (Cricetulus griseus), [10] zebrafish (Danio rerio), [11] horse (Equus caballus), [12] Takifugu rubripes , [11] Tetraodon nigroviridis , [11] chicken (Gallus gallus), [13] [14] gray short-tailed opossum (Monodelphis domestica), [15] platypus (Ornithorhynchus anatinus), [16] Japanese medaka (Oryzias latipes), [17] African clawed frog (Xenopus laevis), [18] Tasmanian devil (Sarcophilus harrisii), [19] pig (Sus scrofa) [20] and zebra finch (Taeniopygia guttata). [21] In some of these species the presence of miR-19 microRNAs have been directly measured, in other species genes have been identified with sequences that are predicted to encode miR-19. [1]

Expression

MiR-17-92 cluster was identified to encode 6 single mature miRNA (miR-17, , miR-19, miR-20, miR-92, miR-106) containing the first oncogenic miRNA.

MicroRNA from miR-19 family can be expressed from:

* T-cell acute lymphoblastic leukemia [22]
* B-cell lymphomas [23]
* Cell lines [22]
* Cerebellum [24] [25]
* Purkinje cells [24]
* HeLa cells [26]

Finally they have tissues-specific miRNA expression. These microRNA are considered as oncogenes which improve proliferation, inhibits apoptosis and induce tumor angiogenesis. [27]
These miRNA are context-specific and they have different roles depending on where they are.

miR-19a/b roles

Acute lymphoblastic leukemia

Ectopic expression of miR-19 represses CYLD expression, while miR-19 inhibitor treatment induces CYLD protein expression and decreases NF-kB expression in the downstream signaling pathway. Thus, miR-19, CYLD and NF-kB form a regulatory feedforward loop, which provides new clues for sustained activation of NF-kB in T-cell acute lymphoblastic leukemia. [22]
MiR-19 is sufficient to induce T-cell lymphoblastic leukemia activating Notch1 and accelerate the disease. Its targets are:

* Bim (Bcl2L11) gene
* AMP-activated kinase (Prkaa1) gene
* E2F1 gene
* the tumour suppressor phosphatases PTEN
* PP2A (Ppp2r5e) gene
* Dock5 protein

MiR-19b coordinates a PI3K pathway acting on cell survival in lymphocytes contributing to leukaemogenesis. [28] [29] [30]

This pathway is activated through PTEN loss and can contribute to reduce sensitivity to chemotherapy and (in T-ALL) may impact the effectiveness of therapeutic gamma-secretase inhibitors.

Primary central nervous system lymphoma

Baraniskin and al. study show that miR-21, miR-19, and miR-92a levels in cerebrospinal fluid (CSF) seems to be good biomarkers to diagnose a Primary central nervous system lymphoma (PCNSL). They also demonstrate that miRNAs in plasma are in a resistant form to intrinsic RNase activity, and there is a low RNase activity in the CSF. [25]

B-cell lymphomas

MiR-19 has been identified as a key responsible for the oncogenic activity, reducing the tumor suppressor gene PTEN expression and activating AKT/mTOR pathway. This cluster might be important regulator on cancer and aging. [31] [32]
Mu and al. demonstrated that the expression of endogenous miR-17-92 is required to suppress apoptosis in Myc-driven B-cell lymphomas. More specifically, miR-19a and miR-19b are required and sufficient to recapitulate the oncogenic properties of the entire cluster. [23] [33] Using prediction algorithms, they found miR-19 targets to the pro-survival functions:

* PTEN tumor suppressor gene
* PTEN mRNA
* Sbf2 gene
* Bcl7a gene
* Rnf44 gene

Keratinocytes

In the cell response to stress, the most important is the post-transcriptional control of the important gene expression to cell survival and apoptosis. MiR-19 regulates the Ras homolog B (RhoB) expression in keratinocytes after ultraviolet (UV) radiation exposition. This phenomenon needs the binding of human antigen R (HuR) to the rhoB mRNA 3'-untranslated region. In this case, HuR acts positively on miRNA action. The interaction between HuR and miR-19 with rhoB is lost under UV treatment. Here, miR-19, linked to RhoB, acts like a protector against keratinocyte apoptosis. A 52-nucleotide-long sequence of the rhoB 3'-UTR spanning bases 818–870, containing the miR-19 and the HuR binding site was sufficient for UV regulation. This event is UV dependent! [34]

Multiple myeloma

One study on multiple myeloma patients permitted to identified a selective up-regulation of miR-32 and the miR-17-92 cluster. MiR-19a and miR-19b were shown to down regulate SOCS-1 expression (a specific gene that inhibits IL-6 growth signaling). Therefore, miR-17-92 with miR-21, inhibits apoptosis and promotes cell survival. [33]

Retinoblastoma

In this case, miR-17-92 cluster promotes retinoblastoma due to loss of Rb family members. The mouse retinal development need miR-17-92 over-expression with Rb and p107 deletion, but it occurred frequent emergence of retinoblastoma and metastasis to the brain.
Here, the cluster oncogenic function is not mediated by a miR-19/PTEN axis toward apoptosis suppression like in lymphoma or in leukemia models. MiR-17-92 increase the proliferative capacity of Rb/p107-deficient in retinal cells.
Moreover, the Rb family members deletion led to compensatory up-regulation of the cyclin-dependent kinase inhibitor p21Cip1.
Finally, the cluster over-expression counteracted p21Cip1 up-regulation, promotes proliferation and drove retinoblastoma formation. [35]

Role in normal development of heart, lungs and immune system

Scientists observed that the loss of function of the miR-17-92 cluster is induced in smaller embryos and postnatal deaths. [36] The specific role of this cluster in heart and lung development remains unclear, but the observations described above show that these miRNAs are normally highly expressed in embryonic lung and decrease with maturity. Moreover, transgenic expression of these miRNAs specifically in lung epithelium results in severe developmental defects with enhanced proliferation and inhibition of differentiation of epithelial cells.
Furthermore, mouse hematopoiesis occurring in the absence of miR-17-92 leads to an isolated defect in B cell development. [36]

Role in the endothelial differentiation of stem cells

The miR-17-92 cluster containing miR-19 miRNA family is also involved into control endothelial cell functions and neo-vascularization. MiRNA cluster (miR-17, miR-18, miR-19 and miR-20) increased during the induction of endothelial cell differentiation in embryonic stem cells (tested on murine) or induce pluripotent stem cells. Even though this cluster regulates vascular integrity and angiogenesis, none of each members has a significant impact on the endothelial differentiation of pluripotent stem cells. [37]

miR-19a roles

Spinocerebellar ataxia type 1

It has been showing that the 3' UTR of the ATXN1 gene contains 3 target sites for miR-19, and this microRNA shows moderate down regulation of reporter genes containing the ATXN1 3' UTR. Furthermore, it directly binds to the ATXN1 3´UTR to suppress the translation of ATXN1. ATXN1 is also regulated by miR-101, and miR-130. [24]

Breast cancer

MiR-19 regulates tissue factor expression at a post-transcriptional level in breast cancer cells, providing a molecular basis for the selective expression of the tissue factor gene. Thanks to bioinformatics analyses, scientists predicted microRNA-Binding sites for miR-19, miR-20 and miR-106b in the 3'-UTR tissue factor transcript. Experiments confirmed that it negatively regulates gene expression in MCF-7 cells, and over-expression of miR-19 downregulates tissue factor expression in MDA-MB-231 cells (human breast cancer cell lines). The main action of miR-19 seems to inhibit protein translation of the tissue factor gene in less invasive breast cancer cells. [27]

miR-19b roles

Rheumatoid arthritis

MiR-19 also takes part in inflammatory responses enhancing or repressing pro-inflammatory mediators expression. It positively regulates Toll-like receptor signaling with Dicer1 deletion and miRNA depletion. MiR-19b is an important protagonist in this phenomenon, regulating positively NF-kB activity. MiRNA depletion inhibits cytokines production by NF-kB. This indicates that miRNA control of NF-kB signaling repressors thanks to its relief. Some important regulators of NF-kB signaling (like A20 (Tnfaip3), Cyld, and Cézanne (Otud7b)) is targeted by the miR-17-92 cluster.
Moreover, mir-19 targets some members of the Tnfaip3-ubiquitin editing complex (Tnfaip3/Itch/Tnip1/Rnf11). MiR-19 directly involved in the modulation of several NF-kB signaling negative regulators expression, indicating an important role for Rnf11 in the effect of miR-19b on NF-kB signaling.
Finally, miR-19b exacerbates the cells crucial inflammatory activation in rheumatoid arthritis disease. [26] [29]

Related Research Articles

mir-17 microRNA precursor family

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. 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.

mir-1 microRNA precursor family

The miR-1 microRNA precursor is a small micro RNA that regulates its target protein's expression in the cell. microRNAs are transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give products at ~22 nucleotides. In this case the mature sequence comes from the 3' arm of the precursor. The mature products are thought to have regulatory roles through complementarity to mRNA. In humans there are two distinct microRNAs that share an identical mature sequence, and these are called miR-1-1 and miR-1-2.

mir-2 microRNA precursor

The mir-2 microRNA family includes the microRNA genes mir-2 and mir-13. Mir-2 is widespread in invertebrates, and it is the largest family of microRNAs in the model species Drosophila melanogaster. MicroRNAs from this family are produced from the 3' arm of the precursor hairpin. Leaman et al. showed that the miR-2 family regulates cell survival by translational repression of proapoptotic factors. Based on computational prediction of targets, a role in neural development and maintenance has been suggested.

The miR-34 microRNA precursor family are non-coding RNA molecules that, in mammals, give rise to three major mature miRNAs. The miR-34 family members were discovered computationally and later verified experimentally. The precursor miRNA stem-loop is processed in the cytoplasm of the cell, with the predominant miR-34 mature sequence excised from the 5' arm of the hairpin.

mir-92 microRNA precursor family

The miR-92 microRNAs are short single stranded non-protein coding RNA fragments initially discovered incorporated into an RNP complex with a proposed role of processing RNA molecules and further RNP assembly. Mir-92 has been mapped to the human genome as part of a larger cluster at chromosome 13q31.3, where it is 22 nucleotides in length but exists in the genome as part of a longer precursor sequence. There is an exact replica of the mir-92 precursor on the X chromosome. MicroRNAs are endogenous triggers of the RNAi pathway which involves several ribonucleic proteins (RNPs) dedicated to repressing mRNA molecules via translation inhibition and/or induction of mRNA cleavage. miRNAs are themselves matured from their long RNA precursors by ribonucleic proteins as part of a 2 step biogenesis mechanism involving RNA polymerase 2.

mIRN21 Non-coding RNA in the species Homo sapiens

microRNA 21 also known as hsa-mir-21 or miRNA21 is a mammalian microRNA that is encoded by the MIR21 gene.

An oncomir is a microRNA (miRNA) that is associated with cancer. MicroRNAs are short RNA molecules about 22 nucleotides in length. Essentially, miRNAs specifically target certain messenger RNAs (mRNAs) to prevent them from coding for a specific protein. The dysregulation of certain microRNAs (oncomirs) has been associated with specific cancer forming (oncogenic) events. Many different oncomirs have been identified in numerous types of human cancers.

miR-155 Non-coding RNA in the species Homo sapiens

MiR-155 is a microRNA that in humans is encoded by the MIR155 host gene or MIR155HG. MiR-155 plays a role in various physiological and pathological processes. Exogenous molecular control in vivo of miR-155 expression may inhibit malignant growth, viral infections, and enhance the progression of cardiovascular diseases.

mir-145 Non-coding RNA in the species Homo sapiens

In molecular biology, mir-145 microRNA is a short RNA molecule that in humans is encoded by the MIR145 gene. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

mir-184 Non-coding microRNA molecule

In molecular biology, miR-184 microRNA is a short non-coding RNA molecule. MicroRNAs (miRNAs) function as posttranscriptional regulators of expression levels of other genes by several mechanisms. Several targets for miR-184 have been described, including that of mediators of neurological development, apoptosis and it has been suggested that miR-184 plays an essential role in development.

mir-210 microRNA

In molecular biology mir-210 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

miR-138

miR-138 is a family of microRNA precursors found in animals, including humans. MicroRNAs are typically transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~22 nucleotide product. The excised region or, mature product, of the miR-138 precursor is the microRNA mir-138.

miR-27 Family of microRNA precursors found in animals

miR-27 is a family of microRNA precursors found in animals, including humans. MicroRNAs are typically transcribed as ~70 nucleotide precursors and subsequently processed by the Dicer enzyme to give a ~22 nucleotide product. The excised region or, mature product, of the miR-27 precursor is the microRNA mir-27.

miR-214

miR-214 is a vertebrate-specific family of microRNA precursors. The ~22 nucleotide mature miRNA sequence is excised from the precursor hairpin by the enzyme Dicer. This sequence then associates with RISC which effects RNA interference.

In molecular biology, competing endogenous RNAs regulate other RNA transcripts by competing for shared microRNAs (miRNAs). Models for ceRNA regulation describe how changes in the expression of one or multiple miRNA targets alter the number of unbound miRNAs and lead to observable changes in miRNA activity - i.e., the abundance of other miRNA targets. Models of ceRNA regulation differ greatly. Some describe the kinetics of target-miRNA-target interactions, where changes in the expression of one target species sequester one miRNA species and lead to changes in the dysregulation of the other target species. Others attempt to model more realistic cellular scenarios, where multiple RNA targets are affecting multiple miRNAs and where each target pair is co-regulated by multiple miRNA species. Some models focus on mRNA 3' UTRs as targets, and others consider long non-coding RNA targets as well. It's evident that our molecular-biochemical understanding of ceRNA regulation remains incomplete.

In molecular biology mir-365 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

In molecular biology mir-744 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

Anti-miRNA oligonucleotides have many uses in cellular mechanics. These synthetically designed molecules are used to neutralize microRNA (miRNA) function in cells for desired responses. miRNA are complementary sequences to mRNA that are involved in the cleavage of RNA or the suppression of the translation. By controlling the miRNA that regulate mRNAs in cells, AMOs can be used as further regulation as well as for therapeutic treatment for certain cellular disorders. This regulation can occur through a steric blocking mechanism as well as hybridization to miRNA. These interactions, within the body between miRNA and AMOs, can be for therapeutics in disorders in which over/under expression occurs or aberrations in miRNA lead to coding issues. Some of the miRNA linked disorders that are encountered in the humans include cancers, muscular diseases, autoimmune disorders, and viruses. In order to determine the functionality of certain AMOs, the AMO/miRNA binding expression must be measured against the expressions of the isolated miRNA. The direct detection of differing levels of genetic expression allow the relationship between AMOs and miRNAs to be shown. This can be detected through luciferase activity. Understanding the miRNA sequences involved in these diseases can allow us to use anti miRNA Oligonucleotides to disrupt pathways that lead to the under/over expression of proteins of cells that can cause symptoms for these diseases.

miR-324-5p is a microRNA that functions in cell growth, apoptosis, cancer, epilepsy, neuronal differentiation, psychiatric conditions, cardiac disease pathology, and more. As a microRNA, it regulates gene expression through targeting mRNAs. Additionally, miR-324-5p is both an intracellular miRNA, meaning it is commonly found within the microenvironment of the cell, and one of several circulating miRNAs found throughout the body. Its presence throughout the body both within and external to cells may contribute to miR-324-5p's wide array of functions and role in numerous disease pathologies – especially cancer – in various organ systems.

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