![]() ![]() The sgRNA itself is made up of two components: a CRISPR RNA (crRNA) component, which directs the complex by homologous base pairing with the target sequence, and a trans-activating crRNA (tracrRNA) component, which is involved in the maturation of crRNA as well as binding it to the Cas protein. The CRISPR/Cas complex is comprised of an RNA-guided DNA endonuclease (Cas9) and a single guide RNA (sgRNA). It is derived from a prokaryotic immune defence in which foreign viral DNA is recognised and cleaved by the Cas protein. The CRISPR/Cas system is capable of introducing specific genetic changes to cultured cells or animal models of interest. These are just some examples of the known roles for ncRNAs in cancer. Increased expression of the lncRNA MALAT1 correlates with poor prognosis in lung cancer, whereas reduced MALAT1 expression leads to reduced lung cancer cell motility, an indicator of lowered metastatic ability. PTEN is a tumour suppressor gene that also regulates the PI3K/AKT pathway and has a known lncRNA regulator itself, PTENP1. Inhibition of HOTAIR led to downregulation of the PI3K/AKT pathway and MRP1, as well as increased sensitivity to the drug imatinib, a tyrosine kinase inhibitor. HOTAIR is known to interact with members of the PRC2 complex, specifically SUZ12 and EZH2, which are involved in methylation of H3K27. ![]() Upregulation of the lncRNA HOTAIR is linked to poor prognosis and increased metastasis in a number of different tumours in humans, including breast, lung, gastric and pancreatic cancers. A variety of cancer-associated genes (such as p53, p15, and p21 ) are regulated by asRNAs. It is now established that asRNAs play vital roles in numerous cellular processes, such as RNA stability, epigenetic remodelling, translation, altered mRNA splicing and imprinting. Local populations declined more than 80% in the first 5 years after DFT1 discovery, and there was an estimated average decline of 77% across all DFTD-affected populations to 2018. DFTD has had a severe impact on its host population. DFT2 contains a Y chromosome, so originated in a male individual. DFT1 originated in a female devil it has two rearranged X chromosomes and no Y chromosome. Both of these transmissible tumours are derived from neuroectodermal tissues, but cytogenetic and transcriptomic evidence show that they originated independently in different individuals. In 2014, a second DFTD emerged in wild devils (DFT2). It causes death in approximately six months. DFTD is a transmissible facial tumour that is spread primarily by biting behaviour during mating and feeding. DFTD was first observed in wild Tasmanian devils in 1996 (DFT1). In contrast to the relatively innocuous and ancient CTVT is the more recently discovered devil facial tumour disease (DFTD). ![]()
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