Antisense RNA Technology
Antisense RNA (asRNA) is an efficient means for regulating gene expression. Generally, there are two kinds of mechanisms for inhibiting target RNA translation by binding of asRNA: (1) hindering ribosome-binding site interactions with ribosomes and/or (2) stimulation of the degradation of the target RNA by ribonucleases via altering its structure. Desai and Papoutsakis first studied the efficiency of asRNA strategies in C. acetobutylicum by applying artificially designed asRNA. However, design of an effective asRNA is not a simple work. In addition, it is not enough to consider only the association rate between asRNA and target mRNA. It was shown that applying M-fold for structural feature-based asRNA design was an effective way. M-fold is a computational algorithm for predicting secondary structure, based on thermodynamics and structural information derived from the studies of known RNA molecules. In this method, free nucleotides (nucleotides in asRNA molecules that are not involved in intramolecular binding) and components (structural features that contain regions of intramolecular binding called duplex RNA) are recognized as the factors for an asRNA. Constructs of asRNA can be generated and visualized using DNA representation software, such as Gene Construction Kit 2 (Textco, Inc., West Lebanon, New Hampshire). In C. acetobutylicum ATCC824, the downregulated expression of adc, buk, ctfAB, and ptb has been reported as the successful cases of asRNA method [7].
Homology Effects
E. Gerhart H. Wagner, ... Pascale Romby, in Advances in Genetics, 2002
Abstract
Antisense RNA-mediated regulation is widespread in bacteria. Most antisense RNA control systems have been found in plasmids, phages, and transposons. Fewer examples were identified in bacterial chromosomes. This chapter summarizes our current knowledge about antisense RNAs with respect to their occurrence, their biological roles, and their diverse mechanisms of action. Examples of cis- or trans-encoded antisense RNAs are discussed, and their properties compared. Most antisense RNAs are posttranscriptionally acting inhibitors of target genes, but a few examples of activator antisense RNAs are known. The implications of RNA structure on topologically and kinetically favored binding pathways are addressed, and solutions that have evolved to permit productive interactions between intricately folded RNAs are discussed. Finally, we describe how particular properties of individual antisense/target RNA systems match their respective biological roles.
Antisense RNA☆
J.T. Wade, in Reference Module in Life Sciences, 2017
RNA-Encoded Antisense RNAs
Antisense RNAs are conventionally DNA-encoded transcripts. However, it is theoretically possible for antisense RNAs to be transcribed from an RNA template. Such a class of antisense RNA has been identified in cultured human cells. These RNAs are complementary to the 3′ end of a polyadenylated mRNA and include a 5′ polyU sequence. Although the origin of these RNAs is unknown, it is likely that they are transcribed from the 3′ ends of polyadenylated mRNAs by an RNA-dependent RNA polymerase. The function of these RNA-encoded antisense RNAs is unknown.
Antisense RNA and Cancer
Zhiguo Wang, in Cancer and Noncoding RNAs, 2018
Antisense RNA and Carcinogenesis
asRNAs are significantly involved in the generation and development of various types of cancers, either to promote carcinogenesis as “Onco-asRNAs” or to inhibit carcinogenesis as “Ts-asRNAs.” Aberrant expression of asRNAs is associated with various types of malignant tumors. The involvements of asRNAs in tumorigenesis are reflected by expression deregulation of these transcripts and of protein-coding genes that these transcripts regulate. In general, Onco-asRNAs are mostly upregulated in cancerous cells/tissues, whereas Ts-asRNAs are frequently downregulated [66]. Studies have documented the roles of numerous asRNAs in cancer pathology, and that many NATs to the cancer-relevant genes exist such as those encodingp21, p53, E-cadherin, myc, Tie-1, p27KIP1, APC,RB1, NF1, PTEN, CDKN1A, CDKN2A, CDKN2B,BRCA1, BRCA2, VHL, TP63, TP73, ARF, WT1, and MYC