The Long and Short Non-coding RNAs in Cancer Biology

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Although not exhibiting apoptosis, p53 null and mutant p53 cancer cells with reduced levels of SNORA42 also show inhibited proliferation and growth, suggesting that SNORA42 knockdown can inhibit cell proliferation in pdependent or -independent manner. In , Wu and coworkers demonstrated that the expression of snoRNAs 5S was differentially displayed in different tissues and noticeably was highly expressed in normal brain, but its expression drastically decreased in meningioma [ ].

Specifically, all these snoRNAs displayed a strong up-regulation in lung tumor specimens and the majority of them is located in commonly frequent genomic amplified regions in lung cancer: SNORD33 is located in chromosome 19q As well as the initial evidence that snoRNAs are involved in cancer development, there are some preliminary data showing that the genes that host snoRNAs might also contribute to the aetiology of this disease.

A research screening for potential tumor-suppressor genes identified that Growth arrest-specific transcript 5 gas5 gene as almost undetectable in actively growing cells but highly expressed in cells undergoing serum starvation or density arrest [ - ]. The first and stronger evidence that GAS5 is related to cancer is the identification that GAS5 transcript levels are significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues and some, but not all, GAS5 transcripts sensitize mammalian cells to apoptosis inducers [ ].

Other studies have also showed that GAS5 reduced expression is associated with poor prognosis in both breast cancer and head and neck squamous cell carcinoma [ ]. Of note, GAS5 has been also identified as a novel partner of the BCL6 in a patient with diffuse large B-cell lymphoma, harboring the t 1;3 q25;q27 [ ]. Taken together, these findings indicates that snoRNA host genes might have important functions in regulating cellular homeostasis and, potentially, cancer biology but more studies are needed to understand their involvement in molecular basis of disease and classify them as sources of potential biomarkers and therapeutic targets.

Another important aspect of the association between snoRNAs and tumorigenesis is represented by the involvement of their associated proteins in cancer. A point mutations in the DKC1 gene is the cause of a rare X-linked recessive disease, the dyskeratosis congenita DC [ - ]. Individuals with DC display features of premature aging, as well as nail dystrophy, mucosal leukoplakia, interstitial fibrosis of the lung, and increased susceptibility to cancer. DKC1 codes for dyskerin, a putative pseudouridine synthase, which carries out two separate functions, both fundamental for proliferating cells.

Dkc1 mutant mice recapitulate the major features of DC, including an increased susceptibility to tumor formation. To this regard, DKC1 was identified as one of only seventy genes that, collectively, constitute a gene expression profile that strongly correlates with the development of aneuploidy and is associated with poor clinical prognosis in a variety of human cancers. Therefore, one hypothesis is that an alteration of physiologic dyskerin function, irrespective of the mechanism, may perturb mitosis and contribute to tumorigenesis but this idea will require more detailed investigation.

Such processing may be of crucial importance, as miRNAs have important roles in the development of many cancers as previously discussed. However, whether this regulation of p53 by miR is relevant to cancer biology has not yet been addressed. Moreover, germline NHP2 and NOP10 mutations give rise to autosomal recessive forms of dyskeratosis congenita, and cancer susceptibility is also a feature of these genetic forms of the disease.

Piwi-interacting RNAs piRNAs are germline-specific small silencing RNAs of 24—30 nt in length, that suppress transposable elements TE activity and maintain genome integrity during germline development, a role highly conserved across animal species [ - ]. TEs are genomic parasites that threaten the genomic integrity of the host genome: they are able to move to new sites by insertion or transposition and thereby disrupt genes and alter the genome [ ].

Any mutations in each of the three members of the PIWI family lead to transposon derepression in the germline, indicating that they act non-redundantly during TE silencing. Initial screening of piRNA sequences revealed that there are hundreds of thousands, if not millions, of individual piRNA sequences [ - ]. Furthermore, they are characterized by the absence of specific sequence motifs or secondary structures such as miRNA precursors. Despite their large diversity, most piRNAs can be mapped to a relatively small number of genomic regions called piRNA clusters.

Each cluster extends from several to more than kilobases, it contains multiple sequences that generate piRNAs and some piRNAs map to both genomic strands, suggesting bidirectional transcription [ - ] Indeed, analysis of piRNA clusters in different Drosophila species has shown that, although the clusters locations are conserved, their sequence content has evolved very quickly suggesting adjustments in the piRNAs patrimony in order to suppress new active transposons invading the species.

Two main pathways, highly conserved in many animal species, have been discovered to be responsible for the biogenesis of the piRNAs: the primary pathways and the Ping-Pong amplification Figure 3 [ - ]. Next, the Ping-Pong cycle further shapes the piRNA population by amplifying sequences that target active transposons. It is currently unclear how primary piRNAs are produced from piRNA clusters but it is likely that piRNA precursors are single-stranded and therefore do not require Dicer for their processing.

Several additional proteins e. In some cell types, such as somatic follicle cells of the D. However, in germline cells of the D. This process results in the generation of repeated rounds of piRNA production having exactly the same sequence of the original primary piRNA. The ping-pong pathway amplifies piRNAs in D. This two steps of piRNA biogenesis can be compared with the function of the adaptive immune system in protecting against pathogens.

The primary piRNA biogenesis pathway resembles the initial generation of the hypervariable antibody repertoire, whereas the amplification loop is analogous to antigen-directed clonal expansion of antibody-producing lymphocytes during the acute immune response. In fact, HIWI maps to a locus known as a germ cell tumor susceptibility locus 12aq HIWI overexpression has also been found in somatic cells such as soft-tissue sarcomas or ductal pancreas adenocarcinoma, and strongly correlates with bad prognosis and high incidence of tumor-related death, providing an example for a potential tumorigenic role of a piRNA-related protein in somatic cells [ , ].

In some cancers, PIWIL2 overexpression has been suggested to induced resistance in cells to cisplatin, which might arise because of increased chromatin condensation that prevents the normal process of DNA repair [ ]. Furthermore, new high-throughput sequencing data revealed the presence of piRNAs in somotic cells, such as HeLa cells. These somatic piRNAs appear located in the nucleolus and in the cytoplasmic area surrounding the nuclear envolope and in contrast with the large population of known piRNAs in male germ cells, this population of piRNAs is dramatically smaller [ ].

Another example is represented by the downregulation of piR in gastric cancer tissues; its enforced expression inhibited gastric cancer cell growth in vitro and in vivo, suggesting a tumor suppressive properties for piR [ ]. Interestingly, piRNAs not are only involved in direct regulation by degradation of TE but they have also been linked to DNA methylation of the retrotraspon regions, extending piRNA functions beyond post-transcriptional silencing. Specifically, mice with defective PIWI proteins fail to establish de novo methylation of TE sequences during spermatogenesis, leading to the hypothesis that the piRISC can also guide the de novo methylation machinery to TE loci.

In this scenerio, piRNAs may present a perfect guide for discriminating TE sequences from normal protein-coding genes and marking them for DNA methylation; however, the biochemical details of how these two mechanisms of piRNA action might be linked have not yet been revealed [ , ]. All together, these data revealed that PIWI-associated RNAs and PIWI pathway has a more profound function outside germline cells than was originally thought but many more studies are needed to clarify their specific role in tumorigenesis.

A, schematic representation of the Drosophila egg chamber. B,piRNAs which are 24—32 nt in length are processed from single-stranded RNA precursors that are transcribed largely from mono- or bidirectional intergenic repetitive elements known as piRNA clusters. First, primary piRNAs are produced through the primary processing pathway and are amplified through the ping-pong pathway, which requires Slicer activity of PIWI proteins.

Subsequently, additional piRNAs are produced through a PIWI-protein-catalysed amplification loop called the 'ping-pong cycle' via sense and antisense intermediates. Given their unexpected abundance, lncRNAs were initially thought to be spurious transcriptional noise resulting from low RNA polymerase fidelity [ ]. However, the restricted expression of many long ncRNAs to particular developmental contexts, the often exhibiting precise subcellular localization and the binding of transcription factors to non-coding loci, suggested that a significant portion of ncRNAs fulfills functional roles beyond transcriptional remodelling [ - ].

Non-Coding RNAs and Cancer

One main characteristic of the lncRNAs is their very low sequence conservation that had fueled the idea that they are not functional. This assertion needs to be carefully considered and takes in consideration several points. First, a recent study identified the presence of 1, lncRNAs that show a strong evolutionary conservation and function ranging from from embryonic stem cell pluripotency to cell proliferation [ ].

In contrast to the protein coding genes, long ncRNAs can exhibit shorter stretches of sequence that are conserved to maintain functional domains and structures. Indeed, many long ncRNAs with a known function, such as Xist , only exhibit high conservation over short sections of their length [ ]. Third, rather than being indicative of non-functionality, low sequence conservation can also be explained by high rates of primary sequence evolution if long ncRNAs have, like promoters and other regulatory elements, more plastic structure—function constraints than proteins [ ].

Although the specific molecular mechanisms are not defined, there are several examples that can illustrate the silencing potential of lncRNAs Figure 4. Another important example is represented by the hundreds of long ncRNAs which are sequentially expressed along the temporal and spatial developmental axes of the human homeobox Hox loci, where they define chromatin domains of differential histone methylation and RNA polymerase accessibility [ ]. This model fits other chromatin modifying complexes, such as Mll, PcG, and G9a methyltransferase, which can be similarly directed by their associated ncRNAs [ ].

In fact, HOTAIR is upregulated in breast carcinoma and colon cancer and its correlates with metastasis and poor prognosis [ ] Enforced expression of HOTAIR consistently changed the pattern of occupancy of Polycomb proteins from the typical epithelial mammary cells pattern to that of embryonic fibroblasts [ ]. Many other tumor suppressor genes that are frequently silenced by epigenetic mechanisms in cancer also have antisense partners, which can affect gene expression with different other mechanism.

Expression of the ncRNA prevents the splicing of the intron that contains an internal ribosome entry site required for efficient translation and expression of the ZEB2 protein with a further efficient translation Figure 4. In this context, it has been evaluated that the prevalence of lncRNAs are antisense to introns, hypothesizing their role in the regulation of splicing or capable of generating mRNA duplexes that fuel the RISC machinery to silence gene expression. One major emergent theme is the involvement of the lncRNAs in the assembly or activity of transcription factors functioning as a scaffold for the docking of many proteins, mimicking functional DNA elements or modulation of PolII itself.

Schematic representation of the control operated on protein coding gene by the lncRNAs at the level of chromatin remodelling, transcriptional control and post-transcriptional processing. In this case, the lncRNA recruits the Polycomb complex by inducing trimethylation of the lysine 27 residues me3K27 of histone H3 to produce heterochromatin formation and repress gene expression. Second, an ultraconserved enhancer is transcribed as a long ncRNA, Evf2, which subsequently acts as a co-activator to the transcription factor DLX2, to regulate the Dlx6 gene transcription.

This retention results in an efficient Zeb2 translation related to the presence of an internal ribosome entry site IRE in the retained intron. The modified and promoter-docked TLS inhibits the histone acetyltransferase activities of CReB binding protein and p inducing the silencing of cyclin D1 expression Figure 4 [ ]. A different co-activator activity mediated by lncRNAs is also evident in the regulation of Dlx genes, important modulators of neuronal development and patterning [ ].

Dlx expression is regulated by two ultraconserved enhancers one of which is transcribed in a lncRNA, named Evf Evf2 forms a stable complex with the homodomein protein DLX-2 which in turn acts as a transcriptional enhancer of Dxl gene Figure 4. In some cases, lncRNAs can also affect RNA polymerase activity by influencing the initiation complex in the choice of the promoter. This could be a widespread mechanism for controlling promoter usage as thousands of triplex structures exist in eukaryotic chromosomes.

Recently, lncRNAs have also shown their tumorigenic potential by modulating the transcriptional program of p53 [ ]. An 3kb lncRNAs, linc-RNA-p21, transcriptionally activated by p53, has been shown to collaborate with p53 in order to control the gene expression in response to DNA damage. Specifically, silencing of lincRNA-p21 derepresses the expression of hundred of genes which are also derepressed following p53 knockdown. The final category of lncRNAs is represented by those molecules capable to generate the formation of compartmentalized nuclear organelles, subnuclear membraneless nuclear bodies whose funtion is relative unknown.

One of them is represented by cell-cycle regulated nuclear foci, named paraspeckles. While depletion of NEAT or Men epsilon disrupts the paraspeckles, their overexpression strongly increases their number.

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There is a number of different lncRNAs that localize to different nuclear regions [ ]. Metastasis-associated lung adenocarcinoma transcript 1 MALAT1 localizes to the splicing speckles, Xist and Kcnq1ot1 both, localize to the perinucleolar region during the S phase of the cell cycle, a class of repeat-associated lncRNAs es SatIII are associated to nuclear stress bodies which are produced on specifc pericentromeric heterochromatic domains containing SatIII gene itself. Over the last decade, a growing number of non-coding transcripts have been found to have roles in gene regulation and RNA processing.

The most well known small non-coding RNAs are the microRNAs, but the network of long and short non-coding transcripts is complex and is likely to contain as yet unidentified classes of molecules that form transcriptional regulatory networks. The field of small and long non coding RNAs is rapidly advancing toward in vivo delivery for therapeutic purposes. Advanced molecular therapies aimed at downmodulating or upmodulating the level of a given miRNA in model organisms have been successfully established. The use of miRNAs is still being evaluated preclinically; no clinical or toxicologic studies have been published but the future is promising.

Kota and collegues reported that systemic administration of this miRNA in a mouse model of HCC using adeno-associated virus AAV results in inhibition of cancer cell proliferation, induction of tumor-specific apoptosis, and dramatic protection from disease progression without toxicity Recently, Pineau et al. They introduced into liver cancer cells, by lipofection, LNA-modified oligonucleotides specifically designed for miR antimiR and miR antimiR knockdown.

Thus the use of synthetic inhibitors of miR may prove to be a promising approach to liver cancer treatment Despite recent progress in silencing of miRNAs in rodents, the development of effective and safe approaches for sequence-specific antagonism of miRNAs in vivo remains a significant scientific and therapeutic challenge. Recently, Elmen and collaborators showed for the first time, that the simple systemic delivery of an unconjugated, PBS-formulated LNA-antimiR effectively antagonizes the liver-expressed miR in nonhuman primates.

Administration by intravenous injections of LNA-antimiR into African green monkeys resulted in the formation of stable heteroduplexes between the LNA-antimiR and miR, accompanied by depletion of mature miR and dose-dependent lowering of plasma cholesterol. These findings demonstrate the utility of systemically administered LNA-antimiRs in exploring miRNA functions in primates and show the impressive potential of this strategy to overcome a major hurdle for clinical miRNA therapy.

In conclusion, the discovery of small RNAs and their functions has revitalized the prospect of controlling expression of specific genes in vivo, with the ultimate hope of building a new class of gene-specific medical therapies. Just how significant are the ncRNAs?

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It seems that ncRNAs were overlooked in the past simply because researchers were specifically looking for RNAs that code proteins. The above discussed data highlight that the complexity of genomic control operated by the ncRNAs is somewhat greater than previously imagined, and that they could represent a total new order of genomic control. In this scenario, understanding the precise roles of ncRNAs is a key challenge.

The targeting of other ncRNAs, in addition to miRNAs, is still in its infancy, but new important developments are expected in this area.

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Therefore, small RNAs could become powerful therapeutic tools in the near future. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers. Login to your personal dashboard for more detailed statistics on your publications. Edited by Yahwardiah Siregar. Edited by Mehmet Gunduz. By Nicole K. Nickerson, Jennifer L. Riese II, Kenneth P. Nephew and John Foley. We are IntechOpen, the world's leading publisher of Open Access books.

Built by scientists, for scientists. Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. Downloaded: Introduction The question of which regions of the human genome constitute its functional elements—those expressed as genes or serving as regulatory elements—has long been a central topic in biology.

MicroRNAs In , Victor Ambros and colleagues discovered a gene, lin-4 , that affected development in Caenorhabditis elegans and found that its product was a small nonprotein-coding RNA [ 31 ]. Table 1. Non coding RNA in human genome. MicroRNAs and cancer Cancer is a multistep process in which normal cells experience genetic changes that progress them through a series of pre-malignant states initiation into invasive cancer progression that can spread throughout the body metastasis.

Table 2. Oncogenic microRNAs Although studies linking miRNA dysfunctions to human diseases are in their infancy, a great deal of data already exists, establishing an important role for miRNAs in the pathogenesis of cancer. Table 3. Table 4. It has been suggested through multiple studies that testis , [7] and neural tissues express the greatest amount of long non-coding RNAs of any tissue type. Big efforts have been put into investigating lncRNAs in plant species, since they remain far more uninvestigated than in mammal species. In the landscape of the mammalian genome was described as numerous 'foci' of transcription that are separated by long stretches of intergenic space.

The GENCODE consortium has collated and analysed a comprehensive set of human lncRNA annotations and their genomic organisation, modifications, cellular locations and tissue expression profiles. There has been considerable debate about whether lncRNAs have been misannotated and do in fact encode proteins. Several lncRNAs have been found to in fact encode for peptides with biologically significant function. However, further investigations into vertebrate lncRNAs revealed that while lncRNAs are conserved in sequence, they are not conserved in transcription.

Some argue that these observations suggest non-functionality of the majority of lncRNAs, [43] [44] [45] while others argue that they may be indicative of rapid species-specific adaptive selection.

Roles of long non-coding RNAs in colorectal cancer tumorigenesis: A Review

While the turnover of lncRNA transcription is much higher than initially expected, it is important to note that still, hundreds of lncRNAs are conserved at the sequence level. There have been several attempts to delineate the different categories of selection signatures seen amongst lncRNAs including: lncRNAs with strong sequence conservation across the entire length of the gene, lncRNAs in which only a portion of the transcript e. Large-scale sequencing of cDNA libraries and more recently transcriptomic sequencing by next generation sequencing indicate that long noncoding RNAs number in the order of tens of thousands in mammals.

However, despite accumulating evidence suggesting that the majority of these are likely to be functional, [52] [53] only a relatively small proportion has been demonstrated to be biologically relevant. As of June , a total of human lncRNAs that with experimental evidences have been community-curated in LncRNAWiki a wiki-based, publicly editable and open-content platform for community curation of human lncRNAs [56] in respect of the functional mechanisms and disease associations, which can also be accessed in LncBook.

In eukaryotes, RNA transcription is a tightly regulated process. NcRNAs modulate the function of transcription factors by several different mechanisms, including functioning themselves as co-regulators, modifying transcription factor activity, or regulating the association and activity of co-regulators. For example, the ncRNA Evf-2 functions as a co-activator for the homeobox transcription factor Dlx2 , which plays important roles in forebrain development and neurogenesis.

The existence of other similar ultra- or highly conserved elements within the mammalian genome that are both transcribed and fulfil enhancer functions suggest Evf-2 may be illustrative of a generalised mechanism that tightly regulates important developmental genes with complex expression patterns during vertebrate growth.

Local ncRNAs can also recruit transcriptional programmes to regulate adjacent protein-coding gene expression. In the broad sense, this mechanism allows the cell to harness RNA-binding proteins, which make up one of the largest classes within the mammalian proteome, and integrate their function in transcriptional programs. Recent evidence has raised the possibility that transcription of genes that escape from X-inactivation might be mediated by expression of long non-coding RNA within the escaping chromosomal domains.

These examples, which bypass specific modes of regulation at individual promoters to mediate changes directly at the level of initiation and elongation transcriptional machinery, provide a means of quickly affecting global changes in gene expression. The ability to quickly mediate global changes is also apparent in the rapid expression of non-coding repetitive sequences. A dissection of the functional sequences within Alu RNA transcripts has drafted a modular structure analogous to the organization of domains in protein transcription factors.

In addition to heat shock , the expression of SINE elements including Alu, B1, and B2 RNAs increases during cellular stress such as viral infection [87] in some cancer cells [88] where they may similarly regulate global changes to gene expression. It was argued that HSR-1 is present in mammalian cells in an inactive state, but upon stress is activated to induce the expression of heat shock genes. The formation of RNA duplexes between complementary ncRNA and mRNA may mask key elements within the mRNA required to bind trans-acting factors, potentially affecting any step in post-transcriptional gene expression including pre-mRNA processing and splicing, transport, translation, and degradation.

The splicing of mRNA can induce its translation and functionally diversify the repertoire of proteins it encodes. Likewise, the expression of an overlapping antisense Rev-ErbAa2 transcript controls the alternative splicing of the thyroid hormone receptor ErbAa2 mRNA to form two antagonistic isoforms.

Long non-coding RNA - Wikipedia

NcRNA may also apply additional regulatory pressures during translation , a property particularly exploited in neurons where the dendritic or axonal translation of mRNA in response to synaptic activity contributes to changes in synaptic plasticity and the remodelling of neuronal networks. Also, long ncRNAs that form extended intramolecular hairpins may be processed into siRNAs, compellingly illustrated by the esi-1 and esi-2 transcripts. However, the generation of endo-siRNAs from antisense transcripts or pseudogenes may also silence the expression of their functional counterparts via RISC effector complexes, acting as an important node that integrates various modes of long and short RNA regulation, as exemplified by the Xist and Tsix see above.

Epigenetic modifications, including histone and DNA methylation, histone acetylation and sumoylation, affect many aspects of chromosomal biology, primarily including regulation of large numbers of genes by remodeling broad chromatin domains. In Drosophila, long ncRNAs induce the expression of the homeotic gene, Ubx, by recruiting and directing the chromatin modifying functions of the trithorax protein Ash1 to Hox regulatory elements.

HOTAIR is thought to achieve this by directing the action of Polycomb chromatin remodeling complexes in trans to govern the cells' epigenetic state and subsequent gene expression. For example, the majority of protein-coding genes have antisense partners, including many tumour suppressor genes that are frequently silenced by epigenetic mechanisms in cancer. Many emergent themes of ncRNA-directed chromatin modification were first apparent within the phenomenon of imprinting , whereby only one allele of a gene is expressed from either the maternal or the paternal chromosome.

In general, imprinted genes are clustered together on chromosomes, suggesting the imprinting mechanism acts upon local chromosome domains rather than individual genes. These clusters are also often associated with long ncRNAs whose expression is correlated with the repression of the linked protein-coding gene on the same allele.

Almost all the genes at the Kcnq1 loci are maternally inherited, except the paternally expressed antisense ncRNA Kcnqot1. The inactivation of a X-chromosome in female placental mammals is directed by one of the earliest and best characterized long ncRNAs, Xist. Xist expression is followed by irreversible layers of chromatin modifications that include the loss of the histone H3K9 acetylation and H3K4 methylation that are associated with active chromatin, and the induction of repressive chromatin modifications including H4 hypoacetylation, H3K27 trimethylation, [] H3K9 hypermethylation and H4K20 monomethylation as well as H2AK monoubiquitylation.

These modifications coincide with the transcriptional silencing of the X-linked genes. Telomeres form the terminal region of mammalian chromosomes and are essential for stability and aging and play central roles in diseases such as cancer. Their association with chromatin, which suggests an involvement in regulating telomere specific heterochromatin modifications, is repressed by SMG proteins that protect chromosome ends from telomere loss.

Recent recognition that long ncRNAs function in various aspects of cell biology has focused increasing attention on their potential to contribute towards disease etiology. The first published report of an alteration in lncRNA abundance in aging and human neurological disease was provided by Lukiw et al. While many association studies have identified unusual expression of long ncRNAs in disease states, there is little understanding of their role in causing disease.

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Expression analyses that compare tumor cells and normal cells have revealed changes in the expression of ncRNAs in several forms of cancer. For example, in prostate tumours, PCGEM1 one of two overexpressed ncRNAs is correlated with increased proliferation and colony formation suggesting an involvement in regulating cell growth.

Overexpression of PRINS is associated with psoriasis susceptibility, with PRINS expression being elevated in the uninvolved epidermis of psoriatic patients compared with both psoriatic lesions and healthy epidermis. Genome-wide profiling revealed that many transcribed non-coding ultraconserved regions exhibit distinct profiles in various human cancer states. Further analysis of one ultraconserved ncRNA suggested it behaved like an oncogene by mitigating apoptosis and subsequently expanding the number of malignant cells in colorectal cancers.

It seems likely that the aberrant expression of these ultraconserved ncRNAs within malignant processes results from important functions they fulfil in normal human development. Recently, a number of association studies examining single nucleotide polymorphisms SNPs associated with disease states have been mapped to long ncRNAs.

The complexity of the transcriptome, and our evolving understanding of its structure may inform a reinterpretation of the functional basis for many natural polymorphisms associated with disease states. Many SNPs associated with certain disease conditions are found within non-coding regions and the complex networks of non-coding transcription within these regions make it particularly difficult to elucidate the functional effects of polymorphisms. The ability of long ncRNAs to regulate associated protein-coding genes may contribute to disease if misexpression of a long ncRNA deregulates a protein coding gene with clinical significance.

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