Pub Date : 2019-04-16DOI: 10.5772/intechopen.84270
F. Guisier, M. Barros-Filho, Leigha D. Rock, F. B. Constantino, Brenda C Minatel, Adam P Sage, E. Marshall, Victor D. Martinez, W. Lam
Despite an inability to encode proteins, small noncoding RNAs (sncRNAs) have critical functions in the regulation of gene expression. They have demonstrated roles in cancer development and progression and are frequently dysregulated. Here we review the biogenesis and mechanism of action, expression patterns, and detection methods of two types of sncRNAs frequently described in cancer: miRNAs and piRNAs. Both miRNAs and piRNAs have been observed to play both oncogenic and tumor-suppressive roles, with miRNAs acting to directly regulate the mRNA of key cancer-associated genes, while piRNAs play crucial roles in maintaining the integrity of the epigenetic landscape. Elucidating these important functions of sncRNAs in normal and cancer biology relies on numerous in silico workflows and tools to profile sncRNA expression. Thus, we also discuss the key detection methods for cancerrelevant sncRNAs, including the discovery of genes that have yet to be described.
{"title":"Small Noncoding RNA Expression in Cancer","authors":"F. Guisier, M. Barros-Filho, Leigha D. Rock, F. B. Constantino, Brenda C Minatel, Adam P Sage, E. Marshall, Victor D. Martinez, W. Lam","doi":"10.5772/intechopen.84270","DOIUrl":"https://doi.org/10.5772/intechopen.84270","url":null,"abstract":"Despite an inability to encode proteins, small noncoding RNAs (sncRNAs) have critical functions in the regulation of gene expression. They have demonstrated roles in cancer development and progression and are frequently dysregulated. Here we review the biogenesis and mechanism of action, expression patterns, and detection methods of two types of sncRNAs frequently described in cancer: miRNAs and piRNAs. Both miRNAs and piRNAs have been observed to play both oncogenic and tumor-suppressive roles, with miRNAs acting to directly regulate the mRNA of key cancer-associated genes, while piRNAs play crucial roles in maintaining the integrity of the epigenetic landscape. Elucidating these important functions of sncRNAs in normal and cancer biology relies on numerous in silico workflows and tools to profile sncRNA expression. Thus, we also discuss the key detection methods for cancerrelevant sncRNAs, including the discovery of genes that have yet to be described.","PeriodicalId":285697,"journal":{"name":"Gene Expression Profiling in Cancer","volume":"35 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122643720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-03-12DOI: 10.5772/INTECHOPEN.83549
C. Siddoo-Atwal
Recently, it has become apparent that the pathogenesis of cancer is closely connected with aberrantly regulated apoptotic cell death and the resulting deregulation of cell proliferation. The loss of equilibrium between cell proliferation and cell death in a tissue may play a crucial role in tumor formation. In fact, the initiation of uncontrolled apoptosis in a tissue may serve as the trigger for carcinogenesis. Various laboratory studies on animals and certain human data are suggestive that tumor formation requires at least two discrete events to take place in response to a carcinogen according to this apoptotic model of carcinogenesis. The first involves an elevation of apoptosis in a particular tissue due to a genetic predisposition, stress, or mutation. The second confers resistance to apoptosis in that same tissue resulting in the formation of an abnormal growth due to a dysregulation of cell number homeostasis. The apoptotic response of each individual to any given carcinogenic or other environmental stimulus is determined by their unique double set of genes inherited from both parents. The singular genetic traits and biochemistry of each individual are attributable solely to this unique combination of genes and their specific regulation. A general example of genetic regulation, gene dose, and control is provided by β -thalassemia point mutations in the beta-globin gene, which confer a blood disease mainly in Mediterranean populations. This mutation (heterozygous and homozygous, at one or both genetic loci) can cause a hereditary red blood cell anemia. Specific examples in relation to cancer predisposition include various genetic models such as the elevated levels of skin cancer among those with certain polymorphisms or inherited mutations in their DNA repair genes like those associated with the disorder, Xeroderma pigmentosum (XP); the high rate of skin cancer observed in albinos with little or no melanin; and the high incidence of lymphomas occurring in patients with the inherited disorder, ataxia-telangiectasia (AT). The mutations associated with each of these conditions can result in an elevated level of apoptosis in the target tissues, either constitutively or in response to particular carcinogens such as UV rays, and can be linked to the initiation of cancer in those specific tissues.
{"title":"Genes That Can Cause Cancer","authors":"C. Siddoo-Atwal","doi":"10.5772/INTECHOPEN.83549","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.83549","url":null,"abstract":"Recently, it has become apparent that the pathogenesis of cancer is closely connected with aberrantly regulated apoptotic cell death and the resulting deregulation of cell proliferation. The loss of equilibrium between cell proliferation and cell death in a tissue may play a crucial role in tumor formation. In fact, the initiation of uncontrolled apoptosis in a tissue may serve as the trigger for carcinogenesis. Various laboratory studies on animals and certain human data are suggestive that tumor formation requires at least two discrete events to take place in response to a carcinogen according to this apoptotic model of carcinogenesis. The first involves an elevation of apoptosis in a particular tissue due to a genetic predisposition, stress, or mutation. The second confers resistance to apoptosis in that same tissue resulting in the formation of an abnormal growth due to a dysregulation of cell number homeostasis. The apoptotic response of each individual to any given carcinogenic or other environmental stimulus is determined by their unique double set of genes inherited from both parents. The singular genetic traits and biochemistry of each individual are attributable solely to this unique combination of genes and their specific regulation. A general example of genetic regulation, gene dose, and control is provided by β -thalassemia point mutations in the beta-globin gene, which confer a blood disease mainly in Mediterranean populations. This mutation (heterozygous and homozygous, at one or both genetic loci) can cause a hereditary red blood cell anemia. Specific examples in relation to cancer predisposition include various genetic models such as the elevated levels of skin cancer among those with certain polymorphisms or inherited mutations in their DNA repair genes like those associated with the disorder, Xeroderma pigmentosum (XP); the high rate of skin cancer observed in albinos with little or no melanin; and the high incidence of lymphomas occurring in patients with the inherited disorder, ataxia-telangiectasia (AT). The mutations associated with each of these conditions can result in an elevated level of apoptosis in the target tissues, either constitutively or in response to particular carcinogens such as UV rays, and can be linked to the initiation of cancer in those specific tissues.","PeriodicalId":285697,"journal":{"name":"Gene Expression Profiling in Cancer","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130688130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-02-19DOI: 10.5772/INTECHOPEN.84462
Katerina Pierouli, Thanasis Mitsis, Eleni D Papakonstantinou, D. Vlachakis
According to the central dogma of molecular biology, the entire process of producing proteins in cells is defined as gene expression, which includes replication of the DNA, DNA transcription into mRNA, and mRNA translation into proteins [1]. Although DNA is the same in all cell types of an organism, each cell expresses only a part of its genes each time, which equates to the ability of the cell to modify the expression of its genome and thus changes its functions [2]. Gene expression profiling is a process in which the genes expressed in a cell can be measured at a specific time [3]. This method simultaneously calculates the levels of thousands of genes leading to the presentation of the expression pattern of the cell’s genes [4]. Therefore, through gene expression profiling, we can discover the functions of a cell at a particular time, which constitutes an important application of this method in cancer cells. A cancer cell is defined as each cell of a tissue in which there is a loss of the standard controlling mechanisms of cell division, resulting in its uncontrolled multiplication, leading to the accumulation of transformed somatic cells, which contain many genetic alterations and epigenetic modifications. These cells have the ability to filter into adjacent tissues, creating metastasis. Metastatic cells impede the physiologic functioning of the vital organs and destroy the physiological tissues resulting in death [5].
{"title":"Introductory Chapter: Gene Profiling in Cancer in the Era of Metagenomics and Precision Medicine","authors":"Katerina Pierouli, Thanasis Mitsis, Eleni D Papakonstantinou, D. Vlachakis","doi":"10.5772/INTECHOPEN.84462","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.84462","url":null,"abstract":"According to the central dogma of molecular biology, the entire process of producing proteins in cells is defined as gene expression, which includes replication of the DNA, DNA transcription into mRNA, and mRNA translation into proteins [1]. Although DNA is the same in all cell types of an organism, each cell expresses only a part of its genes each time, which equates to the ability of the cell to modify the expression of its genome and thus changes its functions [2]. Gene expression profiling is a process in which the genes expressed in a cell can be measured at a specific time [3]. This method simultaneously calculates the levels of thousands of genes leading to the presentation of the expression pattern of the cell’s genes [4]. Therefore, through gene expression profiling, we can discover the functions of a cell at a particular time, which constitutes an important application of this method in cancer cells. A cancer cell is defined as each cell of a tissue in which there is a loss of the standard controlling mechanisms of cell division, resulting in its uncontrolled multiplication, leading to the accumulation of transformed somatic cells, which contain many genetic alterations and epigenetic modifications. These cells have the ability to filter into adjacent tissues, creating metastasis. Metastatic cells impede the physiologic functioning of the vital organs and destroy the physiological tissues resulting in death [5].","PeriodicalId":285697,"journal":{"name":"Gene Expression Profiling in Cancer","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126615400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-01-24DOI: 10.5772/INTECHOPEN.81773
Zhijin Li, Weiling Zhao, Maode Wang, Xiaobo Zhou
Accumulating evidence highlights that noncoding RNAs, especially the long noncoding RNAs (lncRNAs), are critical regulators of gene expression in development, differentiation, and human diseases, such as cancers and heart diseases. The regulatory mechanisms of lncRNAs have been categorized into four major archetypes: signals, decoys, scaffolds, and guides. Increasing evidence points that lncRNAs are able to regulate almost every cellular process by their binding to proteins, mRNAs, miRNA, and/or DNAs. In this review, we present the recent research advances about the regulatory mechanisms of lncRNA in gene expression at various levels, including pretranscription, transcription regulation, and posttranscription regulation. We also introduce the interaction between lncRNA and DNA, RNA and protein, and the bioinformatics applications on lncRNA research.
{"title":"The Role of Long Noncoding RNAs in Gene Expression Regulation","authors":"Zhijin Li, Weiling Zhao, Maode Wang, Xiaobo Zhou","doi":"10.5772/INTECHOPEN.81773","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81773","url":null,"abstract":"Accumulating evidence highlights that noncoding RNAs, especially the long noncoding RNAs (lncRNAs), are critical regulators of gene expression in development, differentiation, and human diseases, such as cancers and heart diseases. The regulatory mechanisms of lncRNAs have been categorized into four major archetypes: signals, decoys, scaffolds, and guides. Increasing evidence points that lncRNAs are able to regulate almost every cellular process by their binding to proteins, mRNAs, miRNA, and/or DNAs. In this review, we present the recent research advances about the regulatory mechanisms of lncRNA in gene expression at various levels, including pretranscription, transcription regulation, and posttranscription regulation. We also introduce the interaction between lncRNA and DNA, RNA and protein, and the bioinformatics applications on lncRNA research.","PeriodicalId":285697,"journal":{"name":"Gene Expression Profiling in Cancer","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128368318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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